Regulation of Autophagy of Prostate Cancer Cells by β-Catenin Signaling

Background/Aims: Autophagy is a cellular degradation process for the recycling of damaged or superfluous intracellular compartments to provide an alternative energy source during periods of metabolic stress for maintaining cell homeostasis and viability. Although autophagy in different contexts have...
Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Rongkai Lin [verfasserIn] Jiayu Feng [verfasserIn] Shaoliang Dong [verfasserIn] Runyang Pan [verfasserIn] Huiqiang Zhuang [verfasserIn] Zhenyu Ding [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2015

Schlagwörter:	Autophagy Nitric oxide β-catenin Wnt Prostate cancer

Übergeordnetes Werk:	In: Cellular Physiology and Biochemistry - Cell Physiol Biochem Press GmbH & Co KG, 2002, 35(2015), 3, Seite 926-932
Übergeordnetes Werk:	volume:35 ; year:2015 ; number:3 ; pages:926-932

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc Journal toc

DOI / URN:	10.1159/000369749

Katalog-ID:	DOAJ042253535

Internformat


LEADER	01000caa a22002652 4500
001	DOAJ042253535
003	DE-627
005	20230502135523.0
007	cr uuu---uuuuu
008	230227s2015 xx \|\|\|\|\|o 00\| \|\|eng c
024	7		\|a 10.1159/000369749 \|2 doi
035			\|a (DE-627)DOAJ042253535
035			\|a (DE-599)DOAJ605e2f37d324483e836b47aef7e74f51
040			\|a DE-627 \|b ger \|c DE-627 \|e rakwb
041			\|a eng
050		0	\|a QP1-981
050		0	\|a QD415-436
100	0		\|a Rongkai Lin \|e verfasserin \|4 aut
245	1	0	\|a Regulation of Autophagy of Prostate Cancer Cells by β-Catenin Signaling
264		1	\|c 2015
336			\|a Text \|b txt \|2 rdacontent
337			\|a Computermedien \|b c \|2 rdamedia
338			\|a Online-Ressource \|b cr \|2 rdacarrier
520			\|a Background/Aims: Autophagy is a cellular degradation process for the recycling of damaged or superfluous intracellular compartments to provide an alternative energy source during periods of metabolic stress for maintaining cell homeostasis and viability. Although autophagy in different contexts have been shown to use similar signaling pathways, the exact molecular regulation of autophagy has been found to be cell-type dependent. Methods: We used rapamycin to trigger autophagy and used nitric oxide (NO) to inhibit autophagy in prostate cancer cells. IWP-2 was used to inhibit β-catenin signaling. Autophagy-associated proteins were examined by Western blot. Results: We found that nitric oxide (NO), a potent cellular messenger, impaired rapamycin-induced autophagy in prostate cancer cells. Further analyses showed that NO induced nuclear accumulation of β-catenin, a key factor of Wnt signaling pathway, to inhibit autophagy in prostate cancer cells. Conclusions: We demonstrate involvement of β-catenin signaling in the regulation of autophagy of prostate cancer cells. Our results shed light on a previously unappreciated β-catenin signaling pathway for regulating autophagy in prostate cancer.
650		4	\|a Autophagy
650		4	\|a Nitric oxide
650		4	\|a β-catenin
650		4	\|a Wnt
650		4	\|a Prostate cancer
653		0	\|a Physiology
653		0	\|a Biochemistry
700	0		\|a Jiayu Feng \|e verfasserin \|4 aut
700	0		\|a Shaoliang Dong \|e verfasserin \|4 aut
700	0		\|a Runyang Pan \|e verfasserin \|4 aut
700	0		\|a Huiqiang Zhuang \|e verfasserin \|4 aut
700	0		\|a Zhenyu Ding \|e verfasserin \|4 aut
773	0	8	\|i In \|t Cellular Physiology and Biochemistry \|d Cell Physiol Biochem Press GmbH & Co KG, 2002 \|g 35(2015), 3, Seite 926-932 \|w (DE-627)300189702 \|w (DE-600)1482056-0 \|x 14219778 \|7 nnns
773	1	8	\|g volume:35 \|g year:2015 \|g number:3 \|g pages:926-932
856	4	0	\|u https://doi.org/10.1159/000369749 \|z kostenfrei
856	4	0	\|u https://doaj.org/article/605e2f37d324483e836b47aef7e74f51 \|z kostenfrei
856	4	0	\|u http://www.karger.com/Article/FullText/369749 \|z kostenfrei
856	4	2	\|u https://doaj.org/toc/1015-8987 \|y Journal toc \|z kostenfrei
856	4	2	\|u https://doaj.org/toc/1421-9778 \|y Journal toc \|z kostenfrei
912			\|a GBV_USEFLAG_A
912			\|a SYSFLAG_A
912			\|a GBV_DOAJ
912			\|a SSG-OLC-PHA
912			\|a GBV_ILN_20
912			\|a GBV_ILN_22
912			\|a GBV_ILN_23
912			\|a GBV_ILN_24
912			\|a GBV_ILN_31
912			\|a GBV_ILN_39
912			\|a GBV_ILN_40
912			\|a GBV_ILN_60
912			\|a GBV_ILN_62
912			\|a GBV_ILN_63
912			\|a GBV_ILN_69
912			\|a GBV_ILN_70
912			\|a GBV_ILN_73
912			\|a GBV_ILN_74
912			\|a GBV_ILN_95
912			\|a GBV_ILN_105
912			\|a GBV_ILN_110
912			\|a GBV_ILN_151
912			\|a GBV_ILN_161
912			\|a GBV_ILN_170
912			\|a GBV_ILN_206
912			\|a GBV_ILN_213
912			\|a GBV_ILN_230
912			\|a GBV_ILN_285
912			\|a GBV_ILN_293
912			\|a GBV_ILN_374
912			\|a GBV_ILN_602
912			\|a GBV_ILN_2014
912			\|a GBV_ILN_2018
912			\|a GBV_ILN_2153
912			\|a GBV_ILN_2885
912			\|a GBV_ILN_2886
912			\|a GBV_ILN_4012
912			\|a GBV_ILN_4037
912			\|a GBV_ILN_4112
912			\|a GBV_ILN_4125
912			\|a GBV_ILN_4126
912			\|a GBV_ILN_4249
912			\|a GBV_ILN_4305
912			\|a GBV_ILN_4306
912			\|a GBV_ILN_4307
912			\|a GBV_ILN_4313
912			\|a GBV_ILN_4322
912			\|a GBV_ILN_4323
912			\|a GBV_ILN_4324
912			\|a GBV_ILN_4325
912			\|a GBV_ILN_4338
912			\|a GBV_ILN_4367
912			\|a GBV_ILN_4700
951			\|a AR
952			\|d 35 \|j 2015 \|e 3 \|h 926-932

Indexfelder

author_variant	r l rl j f jf s d sd r p rp h z hz z d zd
matchkey_str	article:14219778:2015----::euainfuohgopottcneclsy
hierarchy_sort_str	2015
callnumber-subject-code	QP
publishDate	2015
allfields	10.1159/000369749 doi (DE-627)DOAJ042253535 (DE-599)DOAJ605e2f37d324483e836b47aef7e74f51 DE-627 ger DE-627 rakwb eng QP1-981 QD415-436 Rongkai Lin verfasserin aut Regulation of Autophagy of Prostate Cancer Cells by β-Catenin Signaling 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background/Aims: Autophagy is a cellular degradation process for the recycling of damaged or superfluous intracellular compartments to provide an alternative energy source during periods of metabolic stress for maintaining cell homeostasis and viability. Although autophagy in different contexts have been shown to use similar signaling pathways, the exact molecular regulation of autophagy has been found to be cell-type dependent. Methods: We used rapamycin to trigger autophagy and used nitric oxide (NO) to inhibit autophagy in prostate cancer cells. IWP-2 was used to inhibit β-catenin signaling. Autophagy-associated proteins were examined by Western blot. Results: We found that nitric oxide (NO), a potent cellular messenger, impaired rapamycin-induced autophagy in prostate cancer cells. Further analyses showed that NO induced nuclear accumulation of β-catenin, a key factor of Wnt signaling pathway, to inhibit autophagy in prostate cancer cells. Conclusions: We demonstrate involvement of β-catenin signaling in the regulation of autophagy of prostate cancer cells. Our results shed light on a previously unappreciated β-catenin signaling pathway for regulating autophagy in prostate cancer. Autophagy Nitric oxide β-catenin Wnt Prostate cancer Physiology Biochemistry Jiayu Feng verfasserin aut Shaoliang Dong verfasserin aut Runyang Pan verfasserin aut Huiqiang Zhuang verfasserin aut Zhenyu Ding verfasserin aut In Cellular Physiology and Biochemistry Cell Physiol Biochem Press GmbH & Co KG, 2002 35(2015), 3, Seite 926-932 (DE-627)300189702 (DE-600)1482056-0 14219778 nnns volume:35 year:2015 number:3 pages:926-932 https://doi.org/10.1159/000369749 kostenfrei https://doaj.org/article/605e2f37d324483e836b47aef7e74f51 kostenfrei http://www.karger.com/Article/FullText/369749 kostenfrei https://doaj.org/toc/1015-8987 Journal toc kostenfrei https://doaj.org/toc/1421-9778 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_374 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2018 GBV_ILN_2153 GBV_ILN_2885 GBV_ILN_2886 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 35 2015 3 926-932
spelling	10.1159/000369749 doi (DE-627)DOAJ042253535 (DE-599)DOAJ605e2f37d324483e836b47aef7e74f51 DE-627 ger DE-627 rakwb eng QP1-981 QD415-436 Rongkai Lin verfasserin aut Regulation of Autophagy of Prostate Cancer Cells by β-Catenin Signaling 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background/Aims: Autophagy is a cellular degradation process for the recycling of damaged or superfluous intracellular compartments to provide an alternative energy source during periods of metabolic stress for maintaining cell homeostasis and viability. Although autophagy in different contexts have been shown to use similar signaling pathways, the exact molecular regulation of autophagy has been found to be cell-type dependent. Methods: We used rapamycin to trigger autophagy and used nitric oxide (NO) to inhibit autophagy in prostate cancer cells. IWP-2 was used to inhibit β-catenin signaling. Autophagy-associated proteins were examined by Western blot. Results: We found that nitric oxide (NO), a potent cellular messenger, impaired rapamycin-induced autophagy in prostate cancer cells. Further analyses showed that NO induced nuclear accumulation of β-catenin, a key factor of Wnt signaling pathway, to inhibit autophagy in prostate cancer cells. Conclusions: We demonstrate involvement of β-catenin signaling in the regulation of autophagy of prostate cancer cells. Our results shed light on a previously unappreciated β-catenin signaling pathway for regulating autophagy in prostate cancer. Autophagy Nitric oxide β-catenin Wnt Prostate cancer Physiology Biochemistry Jiayu Feng verfasserin aut Shaoliang Dong verfasserin aut Runyang Pan verfasserin aut Huiqiang Zhuang verfasserin aut Zhenyu Ding verfasserin aut In Cellular Physiology and Biochemistry Cell Physiol Biochem Press GmbH & Co KG, 2002 35(2015), 3, Seite 926-932 (DE-627)300189702 (DE-600)1482056-0 14219778 nnns volume:35 year:2015 number:3 pages:926-932 https://doi.org/10.1159/000369749 kostenfrei https://doaj.org/article/605e2f37d324483e836b47aef7e74f51 kostenfrei http://www.karger.com/Article/FullText/369749 kostenfrei https://doaj.org/toc/1015-8987 Journal toc kostenfrei https://doaj.org/toc/1421-9778 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_374 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2018 GBV_ILN_2153 GBV_ILN_2885 GBV_ILN_2886 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 35 2015 3 926-932
allfields_unstemmed	10.1159/000369749 doi (DE-627)DOAJ042253535 (DE-599)DOAJ605e2f37d324483e836b47aef7e74f51 DE-627 ger DE-627 rakwb eng QP1-981 QD415-436 Rongkai Lin verfasserin aut Regulation of Autophagy of Prostate Cancer Cells by β-Catenin Signaling 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background/Aims: Autophagy is a cellular degradation process for the recycling of damaged or superfluous intracellular compartments to provide an alternative energy source during periods of metabolic stress for maintaining cell homeostasis and viability. Although autophagy in different contexts have been shown to use similar signaling pathways, the exact molecular regulation of autophagy has been found to be cell-type dependent. Methods: We used rapamycin to trigger autophagy and used nitric oxide (NO) to inhibit autophagy in prostate cancer cells. IWP-2 was used to inhibit β-catenin signaling. Autophagy-associated proteins were examined by Western blot. Results: We found that nitric oxide (NO), a potent cellular messenger, impaired rapamycin-induced autophagy in prostate cancer cells. Further analyses showed that NO induced nuclear accumulation of β-catenin, a key factor of Wnt signaling pathway, to inhibit autophagy in prostate cancer cells. Conclusions: We demonstrate involvement of β-catenin signaling in the regulation of autophagy of prostate cancer cells. Our results shed light on a previously unappreciated β-catenin signaling pathway for regulating autophagy in prostate cancer. Autophagy Nitric oxide β-catenin Wnt Prostate cancer Physiology Biochemistry Jiayu Feng verfasserin aut Shaoliang Dong verfasserin aut Runyang Pan verfasserin aut Huiqiang Zhuang verfasserin aut Zhenyu Ding verfasserin aut In Cellular Physiology and Biochemistry Cell Physiol Biochem Press GmbH & Co KG, 2002 35(2015), 3, Seite 926-932 (DE-627)300189702 (DE-600)1482056-0 14219778 nnns volume:35 year:2015 number:3 pages:926-932 https://doi.org/10.1159/000369749 kostenfrei https://doaj.org/article/605e2f37d324483e836b47aef7e74f51 kostenfrei http://www.karger.com/Article/FullText/369749 kostenfrei https://doaj.org/toc/1015-8987 Journal toc kostenfrei https://doaj.org/toc/1421-9778 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_374 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2018 GBV_ILN_2153 GBV_ILN_2885 GBV_ILN_2886 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 35 2015 3 926-932
allfieldsGer	10.1159/000369749 doi (DE-627)DOAJ042253535 (DE-599)DOAJ605e2f37d324483e836b47aef7e74f51 DE-627 ger DE-627 rakwb eng QP1-981 QD415-436 Rongkai Lin verfasserin aut Regulation of Autophagy of Prostate Cancer Cells by β-Catenin Signaling 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background/Aims: Autophagy is a cellular degradation process for the recycling of damaged or superfluous intracellular compartments to provide an alternative energy source during periods of metabolic stress for maintaining cell homeostasis and viability. Although autophagy in different contexts have been shown to use similar signaling pathways, the exact molecular regulation of autophagy has been found to be cell-type dependent. Methods: We used rapamycin to trigger autophagy and used nitric oxide (NO) to inhibit autophagy in prostate cancer cells. IWP-2 was used to inhibit β-catenin signaling. Autophagy-associated proteins were examined by Western blot. Results: We found that nitric oxide (NO), a potent cellular messenger, impaired rapamycin-induced autophagy in prostate cancer cells. Further analyses showed that NO induced nuclear accumulation of β-catenin, a key factor of Wnt signaling pathway, to inhibit autophagy in prostate cancer cells. Conclusions: We demonstrate involvement of β-catenin signaling in the regulation of autophagy of prostate cancer cells. Our results shed light on a previously unappreciated β-catenin signaling pathway for regulating autophagy in prostate cancer. Autophagy Nitric oxide β-catenin Wnt Prostate cancer Physiology Biochemistry Jiayu Feng verfasserin aut Shaoliang Dong verfasserin aut Runyang Pan verfasserin aut Huiqiang Zhuang verfasserin aut Zhenyu Ding verfasserin aut In Cellular Physiology and Biochemistry Cell Physiol Biochem Press GmbH & Co KG, 2002 35(2015), 3, Seite 926-932 (DE-627)300189702 (DE-600)1482056-0 14219778 nnns volume:35 year:2015 number:3 pages:926-932 https://doi.org/10.1159/000369749 kostenfrei https://doaj.org/article/605e2f37d324483e836b47aef7e74f51 kostenfrei http://www.karger.com/Article/FullText/369749 kostenfrei https://doaj.org/toc/1015-8987 Journal toc kostenfrei https://doaj.org/toc/1421-9778 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_374 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2018 GBV_ILN_2153 GBV_ILN_2885 GBV_ILN_2886 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 35 2015 3 926-932
allfieldsSound	10.1159/000369749 doi (DE-627)DOAJ042253535 (DE-599)DOAJ605e2f37d324483e836b47aef7e74f51 DE-627 ger DE-627 rakwb eng QP1-981 QD415-436 Rongkai Lin verfasserin aut Regulation of Autophagy of Prostate Cancer Cells by β-Catenin Signaling 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background/Aims: Autophagy is a cellular degradation process for the recycling of damaged or superfluous intracellular compartments to provide an alternative energy source during periods of metabolic stress for maintaining cell homeostasis and viability. Although autophagy in different contexts have been shown to use similar signaling pathways, the exact molecular regulation of autophagy has been found to be cell-type dependent. Methods: We used rapamycin to trigger autophagy and used nitric oxide (NO) to inhibit autophagy in prostate cancer cells. IWP-2 was used to inhibit β-catenin signaling. Autophagy-associated proteins were examined by Western blot. Results: We found that nitric oxide (NO), a potent cellular messenger, impaired rapamycin-induced autophagy in prostate cancer cells. Further analyses showed that NO induced nuclear accumulation of β-catenin, a key factor of Wnt signaling pathway, to inhibit autophagy in prostate cancer cells. Conclusions: We demonstrate involvement of β-catenin signaling in the regulation of autophagy of prostate cancer cells. Our results shed light on a previously unappreciated β-catenin signaling pathway for regulating autophagy in prostate cancer. Autophagy Nitric oxide β-catenin Wnt Prostate cancer Physiology Biochemistry Jiayu Feng verfasserin aut Shaoliang Dong verfasserin aut Runyang Pan verfasserin aut Huiqiang Zhuang verfasserin aut Zhenyu Ding verfasserin aut In Cellular Physiology and Biochemistry Cell Physiol Biochem Press GmbH & Co KG, 2002 35(2015), 3, Seite 926-932 (DE-627)300189702 (DE-600)1482056-0 14219778 nnns volume:35 year:2015 number:3 pages:926-932 https://doi.org/10.1159/000369749 kostenfrei https://doaj.org/article/605e2f37d324483e836b47aef7e74f51 kostenfrei http://www.karger.com/Article/FullText/369749 kostenfrei https://doaj.org/toc/1015-8987 Journal toc kostenfrei https://doaj.org/toc/1421-9778 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_374 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2018 GBV_ILN_2153 GBV_ILN_2885 GBV_ILN_2886 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 35 2015 3 926-932
language	English
source	In Cellular Physiology and Biochemistry 35(2015), 3, Seite 926-932 volume:35 year:2015 number:3 pages:926-932
sourceStr	In Cellular Physiology and Biochemistry 35(2015), 3, Seite 926-932 volume:35 year:2015 number:3 pages:926-932
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Autophagy Nitric oxide β-catenin Wnt Prostate cancer Physiology Biochemistry
isfreeaccess_bool	true
container_title	Cellular Physiology and Biochemistry
authorswithroles_txt_mv	Rongkai Lin @@aut@@ Jiayu Feng @@aut@@ Shaoliang Dong @@aut@@ Runyang Pan @@aut@@ Huiqiang Zhuang @@aut@@ Zhenyu Ding @@aut@@
publishDateDaySort_date	2015-01-01T00:00:00Z
hierarchy_top_id	300189702
id	DOAJ042253535
language_de	englisch
fullrecord	<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">DOAJ042253535</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230502135523.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">230227s2015 xx \|\|\|\|\|o 00\| \|\|eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1159/000369749</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)DOAJ042253535</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)DOAJ605e2f37d324483e836b47aef7e74f51</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="050" ind1=" " ind2="0"><subfield code="a">QP1-981</subfield></datafield><datafield tag="050" ind1=" " ind2="0"><subfield code="a">QD415-436</subfield></datafield><datafield tag="100" ind1="0" ind2=" "><subfield code="a">Rongkai Lin</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Regulation of Autophagy of Prostate Cancer Cells by β-Catenin Signaling</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2015</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Background/Aims: Autophagy is a cellular degradation process for the recycling of damaged or superfluous intracellular compartments to provide an alternative energy source during periods of metabolic stress for maintaining cell homeostasis and viability. Although autophagy in different contexts have been shown to use similar signaling pathways, the exact molecular regulation of autophagy has been found to be cell-type dependent. Methods: We used rapamycin to trigger autophagy and used nitric oxide (NO) to inhibit autophagy in prostate cancer cells. IWP-2 was used to inhibit β-catenin signaling. Autophagy-associated proteins were examined by Western blot. Results: We found that nitric oxide (NO), a potent cellular messenger, impaired rapamycin-induced autophagy in prostate cancer cells. Further analyses showed that NO induced nuclear accumulation of β-catenin, a key factor of Wnt signaling pathway, to inhibit autophagy in prostate cancer cells. Conclusions: We demonstrate involvement of β-catenin signaling in the regulation of autophagy of prostate cancer cells. Our results shed light on a previously unappreciated β-catenin signaling pathway for regulating autophagy in prostate cancer.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Autophagy</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Nitric oxide</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">β-catenin</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Wnt</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Prostate cancer</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Physiology</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Biochemistry</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Jiayu Feng</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Shaoliang Dong</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Runyang Pan</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Huiqiang Zhuang</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Zhenyu Ding</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">In</subfield><subfield code="t">Cellular Physiology and Biochemistry</subfield><subfield code="d">Cell Physiol Biochem Press GmbH & Co KG, 2002</subfield><subfield code="g">35(2015), 3, Seite 926-932</subfield><subfield code="w">(DE-627)300189702</subfield><subfield code="w">(DE-600)1482056-0</subfield><subfield code="x">14219778</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:35</subfield><subfield code="g">year:2015</subfield><subfield code="g">number:3</subfield><subfield code="g">pages:926-932</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1159/000369749</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doaj.org/article/605e2f37d324483e836b47aef7e74f51</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">http://www.karger.com/Article/FullText/369749</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="2"><subfield code="u">https://doaj.org/toc/1015-8987</subfield><subfield code="y">Journal toc</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="2"><subfield code="u">https://doaj.org/toc/1421-9778</subfield><subfield code="y">Journal toc</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_DOAJ</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-PHA</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_20</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_22</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_23</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_24</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_31</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_39</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_40</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_60</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_62</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_63</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_69</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_70</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_73</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_74</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_95</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_105</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_110</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_151</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_161</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_170</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_206</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_213</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_230</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_285</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_293</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_374</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_602</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2014</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2018</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2153</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2885</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2886</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4012</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4037</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4112</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4125</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4126</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4249</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4305</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4306</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4307</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4313</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4322</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4323</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4324</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4325</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4338</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4367</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4700</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">35</subfield><subfield code="j">2015</subfield><subfield code="e">3</subfield><subfield code="h">926-932</subfield></datafield></record></collection>
callnumber-first	Q - Science
author	Rongkai Lin
spellingShingle	Rongkai Lin misc QP1-981 misc QD415-436 misc Autophagy misc Nitric oxide misc β-catenin misc Wnt misc Prostate cancer misc Physiology misc Biochemistry Regulation of Autophagy of Prostate Cancer Cells by β-Catenin Signaling
authorStr	Rongkai Lin
ppnlink_with_tag_str_mv	@@773@@(DE-627)300189702
format	electronic Article
delete_txt_mv	keep
author_role	aut aut aut aut aut aut
collection	DOAJ
remote_str	true
callnumber-label	QP1-981
illustrated	Not Illustrated
issn	14219778
topic_title	QP1-981 QD415-436 Regulation of Autophagy of Prostate Cancer Cells by β-Catenin Signaling Autophagy Nitric oxide β-catenin Wnt Prostate cancer
topic	misc QP1-981 misc QD415-436 misc Autophagy misc Nitric oxide misc β-catenin misc Wnt misc Prostate cancer misc Physiology misc Biochemistry
topic_unstemmed	misc QP1-981 misc QD415-436 misc Autophagy misc Nitric oxide misc β-catenin misc Wnt misc Prostate cancer misc Physiology misc Biochemistry
topic_browse	misc QP1-981 misc QD415-436 misc Autophagy misc Nitric oxide misc β-catenin misc Wnt misc Prostate cancer misc Physiology misc Biochemistry
format_facet	Elektronische Aufsätze Aufsätze Elektronische Ressource
format_main_str_mv	Text Zeitschrift/Artikel
carriertype_str_mv	cr
hierarchy_parent_title	Cellular Physiology and Biochemistry
hierarchy_parent_id	300189702
hierarchy_top_title	Cellular Physiology and Biochemistry
isfreeaccess_txt	true
familylinks_str_mv	(DE-627)300189702 (DE-600)1482056-0
title	Regulation of Autophagy of Prostate Cancer Cells by β-Catenin Signaling
ctrlnum	(DE-627)DOAJ042253535 (DE-599)DOAJ605e2f37d324483e836b47aef7e74f51
title_full	Regulation of Autophagy of Prostate Cancer Cells by β-Catenin Signaling
author_sort	Rongkai Lin
journal	Cellular Physiology and Biochemistry
journalStr	Cellular Physiology and Biochemistry
callnumber-first-code	Q
lang_code	eng
isOA_bool	true
recordtype	marc
publishDateSort	2015
contenttype_str_mv	txt
container_start_page	926
author_browse	Rongkai Lin Jiayu Feng Shaoliang Dong Runyang Pan Huiqiang Zhuang Zhenyu Ding
container_volume	35
class	QP1-981 QD415-436
format_se	Elektronische Aufsätze
author-letter	Rongkai Lin
doi_str_mv	10.1159/000369749
author2-role	verfasserin
title_sort	regulation of autophagy of prostate cancer cells by β-catenin signaling
callnumber	QP1-981
title_auth	Regulation of Autophagy of Prostate Cancer Cells by β-Catenin Signaling
abstract	Background/Aims: Autophagy is a cellular degradation process for the recycling of damaged or superfluous intracellular compartments to provide an alternative energy source during periods of metabolic stress for maintaining cell homeostasis and viability. Although autophagy in different contexts have been shown to use similar signaling pathways, the exact molecular regulation of autophagy has been found to be cell-type dependent. Methods: We used rapamycin to trigger autophagy and used nitric oxide (NO) to inhibit autophagy in prostate cancer cells. IWP-2 was used to inhibit β-catenin signaling. Autophagy-associated proteins were examined by Western blot. Results: We found that nitric oxide (NO), a potent cellular messenger, impaired rapamycin-induced autophagy in prostate cancer cells. Further analyses showed that NO induced nuclear accumulation of β-catenin, a key factor of Wnt signaling pathway, to inhibit autophagy in prostate cancer cells. Conclusions: We demonstrate involvement of β-catenin signaling in the regulation of autophagy of prostate cancer cells. Our results shed light on a previously unappreciated β-catenin signaling pathway for regulating autophagy in prostate cancer.
abstractGer	Background/Aims: Autophagy is a cellular degradation process for the recycling of damaged or superfluous intracellular compartments to provide an alternative energy source during periods of metabolic stress for maintaining cell homeostasis and viability. Although autophagy in different contexts have been shown to use similar signaling pathways, the exact molecular regulation of autophagy has been found to be cell-type dependent. Methods: We used rapamycin to trigger autophagy and used nitric oxide (NO) to inhibit autophagy in prostate cancer cells. IWP-2 was used to inhibit β-catenin signaling. Autophagy-associated proteins were examined by Western blot. Results: We found that nitric oxide (NO), a potent cellular messenger, impaired rapamycin-induced autophagy in prostate cancer cells. Further analyses showed that NO induced nuclear accumulation of β-catenin, a key factor of Wnt signaling pathway, to inhibit autophagy in prostate cancer cells. Conclusions: We demonstrate involvement of β-catenin signaling in the regulation of autophagy of prostate cancer cells. Our results shed light on a previously unappreciated β-catenin signaling pathway for regulating autophagy in prostate cancer.
abstract_unstemmed	Background/Aims: Autophagy is a cellular degradation process for the recycling of damaged or superfluous intracellular compartments to provide an alternative energy source during periods of metabolic stress for maintaining cell homeostasis and viability. Although autophagy in different contexts have been shown to use similar signaling pathways, the exact molecular regulation of autophagy has been found to be cell-type dependent. Methods: We used rapamycin to trigger autophagy and used nitric oxide (NO) to inhibit autophagy in prostate cancer cells. IWP-2 was used to inhibit β-catenin signaling. Autophagy-associated proteins were examined by Western blot. Results: We found that nitric oxide (NO), a potent cellular messenger, impaired rapamycin-induced autophagy in prostate cancer cells. Further analyses showed that NO induced nuclear accumulation of β-catenin, a key factor of Wnt signaling pathway, to inhibit autophagy in prostate cancer cells. Conclusions: We demonstrate involvement of β-catenin signaling in the regulation of autophagy of prostate cancer cells. Our results shed light on a previously unappreciated β-catenin signaling pathway for regulating autophagy in prostate cancer.
collection_details	GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_374 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2018 GBV_ILN_2153 GBV_ILN_2885 GBV_ILN_2886 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700
container_issue	3
title_short	Regulation of Autophagy of Prostate Cancer Cells by β-Catenin Signaling
url	https://doi.org/10.1159/000369749 https://doaj.org/article/605e2f37d324483e836b47aef7e74f51 http://www.karger.com/Article/FullText/369749 https://doaj.org/toc/1015-8987 https://doaj.org/toc/1421-9778
remote_bool	true
author2	Jiayu Feng Shaoliang Dong Runyang Pan Huiqiang Zhuang Zhenyu Ding
author2Str	Jiayu Feng Shaoliang Dong Runyang Pan Huiqiang Zhuang Zhenyu Ding
ppnlink	300189702
callnumber-subject	QP - Physiology
mediatype_str_mv	c
isOA_txt	true
hochschulschrift_bool	false
doi_str	10.1159/000369749
callnumber-a	QP1-981
up_date	2024-07-04T00:15:19.105Z
_version_	1803605370845790208
fullrecord_marcxml	<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">DOAJ042253535</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230502135523.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">230227s2015 xx \|\|\|\|\|o 00\| \|\|eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1159/000369749</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)DOAJ042253535</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)DOAJ605e2f37d324483e836b47aef7e74f51</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="050" ind1=" " ind2="0"><subfield code="a">QP1-981</subfield></datafield><datafield tag="050" ind1=" " ind2="0"><subfield code="a">QD415-436</subfield></datafield><datafield tag="100" ind1="0" ind2=" "><subfield code="a">Rongkai Lin</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Regulation of Autophagy of Prostate Cancer Cells by β-Catenin Signaling</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2015</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Background/Aims: Autophagy is a cellular degradation process for the recycling of damaged or superfluous intracellular compartments to provide an alternative energy source during periods of metabolic stress for maintaining cell homeostasis and viability. Although autophagy in different contexts have been shown to use similar signaling pathways, the exact molecular regulation of autophagy has been found to be cell-type dependent. Methods: We used rapamycin to trigger autophagy and used nitric oxide (NO) to inhibit autophagy in prostate cancer cells. IWP-2 was used to inhibit β-catenin signaling. Autophagy-associated proteins were examined by Western blot. Results: We found that nitric oxide (NO), a potent cellular messenger, impaired rapamycin-induced autophagy in prostate cancer cells. Further analyses showed that NO induced nuclear accumulation of β-catenin, a key factor of Wnt signaling pathway, to inhibit autophagy in prostate cancer cells. Conclusions: We demonstrate involvement of β-catenin signaling in the regulation of autophagy of prostate cancer cells. Our results shed light on a previously unappreciated β-catenin signaling pathway for regulating autophagy in prostate cancer.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Autophagy</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Nitric oxide</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">β-catenin</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Wnt</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Prostate cancer</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Physiology</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Biochemistry</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Jiayu Feng</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Shaoliang Dong</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Runyang Pan</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Huiqiang Zhuang</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Zhenyu Ding</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">In</subfield><subfield code="t">Cellular Physiology and Biochemistry</subfield><subfield code="d">Cell Physiol Biochem Press GmbH & Co KG, 2002</subfield><subfield code="g">35(2015), 3, Seite 926-932</subfield><subfield code="w">(DE-627)300189702</subfield><subfield code="w">(DE-600)1482056-0</subfield><subfield code="x">14219778</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:35</subfield><subfield code="g">year:2015</subfield><subfield code="g">number:3</subfield><subfield code="g">pages:926-932</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1159/000369749</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doaj.org/article/605e2f37d324483e836b47aef7e74f51</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">http://www.karger.com/Article/FullText/369749</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="2"><subfield code="u">https://doaj.org/toc/1015-8987</subfield><subfield code="y">Journal toc</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="2"><subfield code="u">https://doaj.org/toc/1421-9778</subfield><subfield code="y">Journal toc</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_DOAJ</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-PHA</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_20</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_22</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_23</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_24</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_31</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_39</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_40</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_60</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_62</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_63</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_69</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_70</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_73</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_74</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_95</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_105</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_110</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_151</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_161</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_170</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_206</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_213</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_230</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_285</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_293</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_374</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_602</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2014</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2018</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2153</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2885</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2886</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4012</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4037</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4112</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4125</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4126</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4249</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4305</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4306</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4307</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4313</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4322</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4323</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4324</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4325</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4338</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4367</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4700</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">35</subfield><subfield code="j">2015</subfield><subfield code="e">3</subfield><subfield code="h">926-932</subfield></datafield></record></collection>
score	7.4014387

Nicht das Richtige dabei?

Schreiben Sie uns!

Regulation of Autophagy of Prostate Cancer Cells by β-Catenin Signaling

Nicht das Richtige dabei?

Zugang & Verfügbarkeit

Vorhandene Bände

Nicht das Richtige dabei?