PARK2 Suppresses Proliferation and Tumorigenicity in Non-small Cell Lung Cancer

Aims:PARK2 mutation is originally associated with the progression of Parkinson's disease. In recent years, PARK2 has been reported as a tumor suppressor gene in various cancers, including lung cancer. However, the biological functions and potential molecular mechanisms of PARK2 in non-small cell lung cancer (NSCLC) are still unclear.Methods: The level of PARK2 expression in 32 tissue samples of NSCLC and matched non-tumor lung tissues was detected by Western blot, and 64 specimens of NSCLC tissues were detected by immunohistochemistry. H1299 and H460 cell lines were used to PARK2 overexpression models, and H460 cell line was also used to PARK2 knockdown model. Using cell viability, colony formation, cell cycle, apoptosis, migration, and invasion assay, the biological functions of PARK2 were evaluated and the potential molecular mechanism of PARK2 was investigated in vitro. Meanwhile, 22 nude mice were employed for in vivo studies.Results: Western blot analysis revealed a decrease of PARK2 protein expression in human NSCLC samples. Immunohistochemistry also identified a vastly reduced expression of PARK2 in NSCLC (72%) and low PARK2 expression was significantly associated with tumor histological grade, lymph node metastasis and advanced TNM stage. Overexpression of PARK2 suppressed cell proliferation, colony formation, migration, and invasion, arrested cell cycle progression in the G1 phase, and induced apoptosis in human non-small cell lines H1299 and H460 in vitro. Meanwhile, knockdown of PARK2 had the opposite biological functions. In addition, PARK2 significantly decreased the tumor volumes in subcutaneous xenograft model and reduced the incidence of metastatic tumors in the transfer model. Exploration of the molecular mechanism of PARK2 in NSCLC showed that PARK2 negatively regulated the EGFR/AKT/mTOR signaling pathway.Conclusions:PARK2 was an important tumor suppressor in NSCLC, which might inhibit cancer growth and metastases through the down regulation of the EGFR/AKT/mTOR signaling pathway. Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Huijie Duan [verfasserIn] Zhong Lei [verfasserIn] Fei Xu [verfasserIn] Tao Pan [verfasserIn] Demin Lu [verfasserIn] Peili Ding [verfasserIn] Chunpeng Zhu [verfasserIn] Chi Pan [verfasserIn] Suzhan Zhang [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2019

Schlagwörter:	PARK2 non-small cell lung cancer proliferation metastasis EGFR/AKT/mTOR

Übergeordnetes Werk:	In: Frontiers in Oncology - Frontiers Media S.A., 2012, 9(2019)
Übergeordnetes Werk:	volume:9 ; year:2019

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.3389/fonc.2019.00790

Katalog-ID:	DOAJ009789391

Internformat


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520			\|a Aims:PARK2 mutation is originally associated with the progression of Parkinson's disease. In recent years, PARK2 has been reported as a tumor suppressor gene in various cancers, including lung cancer. However, the biological functions and potential molecular mechanisms of PARK2 in non-small cell lung cancer (NSCLC) are still unclear.Methods: The level of PARK2 expression in 32 tissue samples of NSCLC and matched non-tumor lung tissues was detected by Western blot, and 64 specimens of NSCLC tissues were detected by immunohistochemistry. H1299 and H460 cell lines were used to PARK2 overexpression models, and H460 cell line was also used to PARK2 knockdown model. Using cell viability, colony formation, cell cycle, apoptosis, migration, and invasion assay, the biological functions of PARK2 were evaluated and the potential molecular mechanism of PARK2 was investigated in vitro. Meanwhile, 22 nude mice were employed for in vivo studies.Results: Western blot analysis revealed a decrease of PARK2 protein expression in human NSCLC samples. Immunohistochemistry also identified a vastly reduced expression of PARK2 in NSCLC (72%) and low PARK2 expression was significantly associated with tumor histological grade, lymph node metastasis and advanced TNM stage. Overexpression of PARK2 suppressed cell proliferation, colony formation, migration, and invasion, arrested cell cycle progression in the G1 phase, and induced apoptosis in human non-small cell lines H1299 and H460 in vitro. Meanwhile, knockdown of PARK2 had the opposite biological functions. In addition, PARK2 significantly decreased the tumor volumes in subcutaneous xenograft model and reduced the incidence of metastatic tumors in the transfer model. Exploration of the molecular mechanism of PARK2 in NSCLC showed that PARK2 negatively regulated the EGFR/AKT/mTOR signaling pathway.Conclusions:PARK2 was an important tumor suppressor in NSCLC, which might inhibit cancer growth and metastases through the down regulation of the EGFR/AKT/mTOR signaling pathway.
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653		0	\|a Neoplasms. Tumors. Oncology. Including cancer and carcinogens
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700	0		\|a Suzhan Zhang \|e verfasserin \|4 aut
700	0		\|a Suzhan Zhang \|e verfasserin \|4 aut
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author_variant	h d hd h d hd z l zl f x fx t p tp d l dl d l dl p d pd c z cz c p cp s z sz s z sz
matchkey_str	article:2234943X:2019----::aksprsepoieainntmrgnctinn
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publishDate	2019
allfields	10.3389/fonc.2019.00790 doi (DE-627)DOAJ009789391 (DE-599)DOAJ574a1e058b4d4f7bbc455032b4ff3a0b DE-627 ger DE-627 rakwb eng RC254-282 Huijie Duan verfasserin aut PARK2 Suppresses Proliferation and Tumorigenicity in Non-small Cell Lung Cancer 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Aims:PARK2 mutation is originally associated with the progression of Parkinson's disease. In recent years, PARK2 has been reported as a tumor suppressor gene in various cancers, including lung cancer. However, the biological functions and potential molecular mechanisms of PARK2 in non-small cell lung cancer (NSCLC) are still unclear.Methods: The level of PARK2 expression in 32 tissue samples of NSCLC and matched non-tumor lung tissues was detected by Western blot, and 64 specimens of NSCLC tissues were detected by immunohistochemistry. H1299 and H460 cell lines were used to PARK2 overexpression models, and H460 cell line was also used to PARK2 knockdown model. Using cell viability, colony formation, cell cycle, apoptosis, migration, and invasion assay, the biological functions of PARK2 were evaluated and the potential molecular mechanism of PARK2 was investigated in vitro. Meanwhile, 22 nude mice were employed for in vivo studies.Results: Western blot analysis revealed a decrease of PARK2 protein expression in human NSCLC samples. Immunohistochemistry also identified a vastly reduced expression of PARK2 in NSCLC (72%) and low PARK2 expression was significantly associated with tumor histological grade, lymph node metastasis and advanced TNM stage. Overexpression of PARK2 suppressed cell proliferation, colony formation, migration, and invasion, arrested cell cycle progression in the G1 phase, and induced apoptosis in human non-small cell lines H1299 and H460 in vitro. Meanwhile, knockdown of PARK2 had the opposite biological functions. In addition, PARK2 significantly decreased the tumor volumes in subcutaneous xenograft model and reduced the incidence of metastatic tumors in the transfer model. Exploration of the molecular mechanism of PARK2 in NSCLC showed that PARK2 negatively regulated the EGFR/AKT/mTOR signaling pathway.Conclusions:PARK2 was an important tumor suppressor in NSCLC, which might inhibit cancer growth and metastases through the down regulation of the EGFR/AKT/mTOR signaling pathway. PARK2 non-small cell lung cancer proliferation metastasis EGFR/AKT/mTOR Neoplasms. Tumors. Oncology. Including cancer and carcinogens Huijie Duan verfasserin aut Zhong Lei verfasserin aut Fei Xu verfasserin aut Tao Pan verfasserin aut Demin Lu verfasserin aut Demin Lu verfasserin aut Peili Ding verfasserin aut Chunpeng Zhu verfasserin aut Chi Pan verfasserin aut Suzhan Zhang verfasserin aut Suzhan Zhang verfasserin aut In Frontiers in Oncology Frontiers Media S.A., 2012 9(2019) (DE-627)684965518 (DE-600)2649216-7 2234943X nnns volume:9 year:2019 https://doi.org/10.3389/fonc.2019.00790 kostenfrei https://doaj.org/article/574a1e058b4d4f7bbc455032b4ff3a0b kostenfrei https://www.frontiersin.org/article/10.3389/fonc.2019.00790/full kostenfrei https://doaj.org/toc/2234-943X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 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_602 GBV_ILN_2003 GBV_ILN_2014 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 9 2019
spelling	10.3389/fonc.2019.00790 doi (DE-627)DOAJ009789391 (DE-599)DOAJ574a1e058b4d4f7bbc455032b4ff3a0b DE-627 ger DE-627 rakwb eng RC254-282 Huijie Duan verfasserin aut PARK2 Suppresses Proliferation and Tumorigenicity in Non-small Cell Lung Cancer 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Aims:PARK2 mutation is originally associated with the progression of Parkinson's disease. In recent years, PARK2 has been reported as a tumor suppressor gene in various cancers, including lung cancer. However, the biological functions and potential molecular mechanisms of PARK2 in non-small cell lung cancer (NSCLC) are still unclear.Methods: The level of PARK2 expression in 32 tissue samples of NSCLC and matched non-tumor lung tissues was detected by Western blot, and 64 specimens of NSCLC tissues were detected by immunohistochemistry. H1299 and H460 cell lines were used to PARK2 overexpression models, and H460 cell line was also used to PARK2 knockdown model. Using cell viability, colony formation, cell cycle, apoptosis, migration, and invasion assay, the biological functions of PARK2 were evaluated and the potential molecular mechanism of PARK2 was investigated in vitro. Meanwhile, 22 nude mice were employed for in vivo studies.Results: Western blot analysis revealed a decrease of PARK2 protein expression in human NSCLC samples. Immunohistochemistry also identified a vastly reduced expression of PARK2 in NSCLC (72%) and low PARK2 expression was significantly associated with tumor histological grade, lymph node metastasis and advanced TNM stage. Overexpression of PARK2 suppressed cell proliferation, colony formation, migration, and invasion, arrested cell cycle progression in the G1 phase, and induced apoptosis in human non-small cell lines H1299 and H460 in vitro. Meanwhile, knockdown of PARK2 had the opposite biological functions. In addition, PARK2 significantly decreased the tumor volumes in subcutaneous xenograft model and reduced the incidence of metastatic tumors in the transfer model. Exploration of the molecular mechanism of PARK2 in NSCLC showed that PARK2 negatively regulated the EGFR/AKT/mTOR signaling pathway.Conclusions:PARK2 was an important tumor suppressor in NSCLC, which might inhibit cancer growth and metastases through the down regulation of the EGFR/AKT/mTOR signaling pathway. PARK2 non-small cell lung cancer proliferation metastasis EGFR/AKT/mTOR Neoplasms. Tumors. Oncology. Including cancer and carcinogens Huijie Duan verfasserin aut Zhong Lei verfasserin aut Fei Xu verfasserin aut Tao Pan verfasserin aut Demin Lu verfasserin aut Demin Lu verfasserin aut Peili Ding verfasserin aut Chunpeng Zhu verfasserin aut Chi Pan verfasserin aut Suzhan Zhang verfasserin aut Suzhan Zhang verfasserin aut In Frontiers in Oncology Frontiers Media S.A., 2012 9(2019) (DE-627)684965518 (DE-600)2649216-7 2234943X nnns volume:9 year:2019 https://doi.org/10.3389/fonc.2019.00790 kostenfrei https://doaj.org/article/574a1e058b4d4f7bbc455032b4ff3a0b kostenfrei https://www.frontiersin.org/article/10.3389/fonc.2019.00790/full kostenfrei https://doaj.org/toc/2234-943X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 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_602 GBV_ILN_2003 GBV_ILN_2014 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 9 2019
allfields_unstemmed	10.3389/fonc.2019.00790 doi (DE-627)DOAJ009789391 (DE-599)DOAJ574a1e058b4d4f7bbc455032b4ff3a0b DE-627 ger DE-627 rakwb eng RC254-282 Huijie Duan verfasserin aut PARK2 Suppresses Proliferation and Tumorigenicity in Non-small Cell Lung Cancer 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Aims:PARK2 mutation is originally associated with the progression of Parkinson's disease. In recent years, PARK2 has been reported as a tumor suppressor gene in various cancers, including lung cancer. However, the biological functions and potential molecular mechanisms of PARK2 in non-small cell lung cancer (NSCLC) are still unclear.Methods: The level of PARK2 expression in 32 tissue samples of NSCLC and matched non-tumor lung tissues was detected by Western blot, and 64 specimens of NSCLC tissues were detected by immunohistochemistry. H1299 and H460 cell lines were used to PARK2 overexpression models, and H460 cell line was also used to PARK2 knockdown model. Using cell viability, colony formation, cell cycle, apoptosis, migration, and invasion assay, the biological functions of PARK2 were evaluated and the potential molecular mechanism of PARK2 was investigated in vitro. Meanwhile, 22 nude mice were employed for in vivo studies.Results: Western blot analysis revealed a decrease of PARK2 protein expression in human NSCLC samples. Immunohistochemistry also identified a vastly reduced expression of PARK2 in NSCLC (72%) and low PARK2 expression was significantly associated with tumor histological grade, lymph node metastasis and advanced TNM stage. Overexpression of PARK2 suppressed cell proliferation, colony formation, migration, and invasion, arrested cell cycle progression in the G1 phase, and induced apoptosis in human non-small cell lines H1299 and H460 in vitro. Meanwhile, knockdown of PARK2 had the opposite biological functions. In addition, PARK2 significantly decreased the tumor volumes in subcutaneous xenograft model and reduced the incidence of metastatic tumors in the transfer model. Exploration of the molecular mechanism of PARK2 in NSCLC showed that PARK2 negatively regulated the EGFR/AKT/mTOR signaling pathway.Conclusions:PARK2 was an important tumor suppressor in NSCLC, which might inhibit cancer growth and metastases through the down regulation of the EGFR/AKT/mTOR signaling pathway. PARK2 non-small cell lung cancer proliferation metastasis EGFR/AKT/mTOR Neoplasms. Tumors. Oncology. Including cancer and carcinogens Huijie Duan verfasserin aut Zhong Lei verfasserin aut Fei Xu verfasserin aut Tao Pan verfasserin aut Demin Lu verfasserin aut Demin Lu verfasserin aut Peili Ding verfasserin aut Chunpeng Zhu verfasserin aut Chi Pan verfasserin aut Suzhan Zhang verfasserin aut Suzhan Zhang verfasserin aut In Frontiers in Oncology Frontiers Media S.A., 2012 9(2019) (DE-627)684965518 (DE-600)2649216-7 2234943X nnns volume:9 year:2019 https://doi.org/10.3389/fonc.2019.00790 kostenfrei https://doaj.org/article/574a1e058b4d4f7bbc455032b4ff3a0b kostenfrei https://www.frontiersin.org/article/10.3389/fonc.2019.00790/full kostenfrei https://doaj.org/toc/2234-943X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 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_602 GBV_ILN_2003 GBV_ILN_2014 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 9 2019
allfieldsGer	10.3389/fonc.2019.00790 doi (DE-627)DOAJ009789391 (DE-599)DOAJ574a1e058b4d4f7bbc455032b4ff3a0b DE-627 ger DE-627 rakwb eng RC254-282 Huijie Duan verfasserin aut PARK2 Suppresses Proliferation and Tumorigenicity in Non-small Cell Lung Cancer 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Aims:PARK2 mutation is originally associated with the progression of Parkinson's disease. In recent years, PARK2 has been reported as a tumor suppressor gene in various cancers, including lung cancer. However, the biological functions and potential molecular mechanisms of PARK2 in non-small cell lung cancer (NSCLC) are still unclear.Methods: The level of PARK2 expression in 32 tissue samples of NSCLC and matched non-tumor lung tissues was detected by Western blot, and 64 specimens of NSCLC tissues were detected by immunohistochemistry. H1299 and H460 cell lines were used to PARK2 overexpression models, and H460 cell line was also used to PARK2 knockdown model. Using cell viability, colony formation, cell cycle, apoptosis, migration, and invasion assay, the biological functions of PARK2 were evaluated and the potential molecular mechanism of PARK2 was investigated in vitro. Meanwhile, 22 nude mice were employed for in vivo studies.Results: Western blot analysis revealed a decrease of PARK2 protein expression in human NSCLC samples. Immunohistochemistry also identified a vastly reduced expression of PARK2 in NSCLC (72%) and low PARK2 expression was significantly associated with tumor histological grade, lymph node metastasis and advanced TNM stage. Overexpression of PARK2 suppressed cell proliferation, colony formation, migration, and invasion, arrested cell cycle progression in the G1 phase, and induced apoptosis in human non-small cell lines H1299 and H460 in vitro. Meanwhile, knockdown of PARK2 had the opposite biological functions. In addition, PARK2 significantly decreased the tumor volumes in subcutaneous xenograft model and reduced the incidence of metastatic tumors in the transfer model. Exploration of the molecular mechanism of PARK2 in NSCLC showed that PARK2 negatively regulated the EGFR/AKT/mTOR signaling pathway.Conclusions:PARK2 was an important tumor suppressor in NSCLC, which might inhibit cancer growth and metastases through the down regulation of the EGFR/AKT/mTOR signaling pathway. PARK2 non-small cell lung cancer proliferation metastasis EGFR/AKT/mTOR Neoplasms. Tumors. Oncology. Including cancer and carcinogens Huijie Duan verfasserin aut Zhong Lei verfasserin aut Fei Xu verfasserin aut Tao Pan verfasserin aut Demin Lu verfasserin aut Demin Lu verfasserin aut Peili Ding verfasserin aut Chunpeng Zhu verfasserin aut Chi Pan verfasserin aut Suzhan Zhang verfasserin aut Suzhan Zhang verfasserin aut In Frontiers in Oncology Frontiers Media S.A., 2012 9(2019) (DE-627)684965518 (DE-600)2649216-7 2234943X nnns volume:9 year:2019 https://doi.org/10.3389/fonc.2019.00790 kostenfrei https://doaj.org/article/574a1e058b4d4f7bbc455032b4ff3a0b kostenfrei https://www.frontiersin.org/article/10.3389/fonc.2019.00790/full kostenfrei https://doaj.org/toc/2234-943X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 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_602 GBV_ILN_2003 GBV_ILN_2014 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 9 2019
allfieldsSound	10.3389/fonc.2019.00790 doi (DE-627)DOAJ009789391 (DE-599)DOAJ574a1e058b4d4f7bbc455032b4ff3a0b DE-627 ger DE-627 rakwb eng RC254-282 Huijie Duan verfasserin aut PARK2 Suppresses Proliferation and Tumorigenicity in Non-small Cell Lung Cancer 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Aims:PARK2 mutation is originally associated with the progression of Parkinson's disease. In recent years, PARK2 has been reported as a tumor suppressor gene in various cancers, including lung cancer. However, the biological functions and potential molecular mechanisms of PARK2 in non-small cell lung cancer (NSCLC) are still unclear.Methods: The level of PARK2 expression in 32 tissue samples of NSCLC and matched non-tumor lung tissues was detected by Western blot, and 64 specimens of NSCLC tissues were detected by immunohistochemistry. H1299 and H460 cell lines were used to PARK2 overexpression models, and H460 cell line was also used to PARK2 knockdown model. Using cell viability, colony formation, cell cycle, apoptosis, migration, and invasion assay, the biological functions of PARK2 were evaluated and the potential molecular mechanism of PARK2 was investigated in vitro. Meanwhile, 22 nude mice were employed for in vivo studies.Results: Western blot analysis revealed a decrease of PARK2 protein expression in human NSCLC samples. Immunohistochemistry also identified a vastly reduced expression of PARK2 in NSCLC (72%) and low PARK2 expression was significantly associated with tumor histological grade, lymph node metastasis and advanced TNM stage. Overexpression of PARK2 suppressed cell proliferation, colony formation, migration, and invasion, arrested cell cycle progression in the G1 phase, and induced apoptosis in human non-small cell lines H1299 and H460 in vitro. Meanwhile, knockdown of PARK2 had the opposite biological functions. In addition, PARK2 significantly decreased the tumor volumes in subcutaneous xenograft model and reduced the incidence of metastatic tumors in the transfer model. Exploration of the molecular mechanism of PARK2 in NSCLC showed that PARK2 negatively regulated the EGFR/AKT/mTOR signaling pathway.Conclusions:PARK2 was an important tumor suppressor in NSCLC, which might inhibit cancer growth and metastases through the down regulation of the EGFR/AKT/mTOR signaling pathway. PARK2 non-small cell lung cancer proliferation metastasis EGFR/AKT/mTOR Neoplasms. Tumors. Oncology. Including cancer and carcinogens Huijie Duan verfasserin aut Zhong Lei verfasserin aut Fei Xu verfasserin aut Tao Pan verfasserin aut Demin Lu verfasserin aut Demin Lu verfasserin aut Peili Ding verfasserin aut Chunpeng Zhu verfasserin aut Chi Pan verfasserin aut Suzhan Zhang verfasserin aut Suzhan Zhang verfasserin aut In Frontiers in Oncology Frontiers Media S.A., 2012 9(2019) (DE-627)684965518 (DE-600)2649216-7 2234943X nnns volume:9 year:2019 https://doi.org/10.3389/fonc.2019.00790 kostenfrei https://doaj.org/article/574a1e058b4d4f7bbc455032b4ff3a0b kostenfrei https://www.frontiersin.org/article/10.3389/fonc.2019.00790/full kostenfrei https://doaj.org/toc/2234-943X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 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_602 GBV_ILN_2003 GBV_ILN_2014 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 9 2019
language	English
source	In Frontiers in Oncology 9(2019) volume:9 year:2019
sourceStr	In Frontiers in Oncology 9(2019) volume:9 year:2019
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	PARK2 non-small cell lung cancer proliferation metastasis EGFR/AKT/mTOR Neoplasms. Tumors. Oncology. Including cancer and carcinogens
isfreeaccess_bool	true
container_title	Frontiers in Oncology
authorswithroles_txt_mv	Huijie Duan @@aut@@ Zhong Lei @@aut@@ Fei Xu @@aut@@ Tao Pan @@aut@@ Demin Lu @@aut@@ Peili Ding @@aut@@ Chunpeng Zhu @@aut@@ Chi Pan @@aut@@ Suzhan Zhang @@aut@@
publishDateDaySort_date	2019-01-01T00:00:00Z
hierarchy_top_id	684965518
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language_de	englisch
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topic_title	RC254-282 PARK2 Suppresses Proliferation and Tumorigenicity in Non-small Cell Lung Cancer PARK2 non-small cell lung cancer proliferation metastasis EGFR/AKT/mTOR
topic	misc RC254-282 misc PARK2 misc non-small cell lung cancer misc proliferation misc metastasis misc EGFR/AKT/mTOR misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens
topic_unstemmed	misc RC254-282 misc PARK2 misc non-small cell lung cancer misc proliferation misc metastasis misc EGFR/AKT/mTOR misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens
topic_browse	misc RC254-282 misc PARK2 misc non-small cell lung cancer misc proliferation misc metastasis misc EGFR/AKT/mTOR misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens
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title	PARK2 Suppresses Proliferation and Tumorigenicity in Non-small Cell Lung Cancer
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title_full	PARK2 Suppresses Proliferation and Tumorigenicity in Non-small Cell Lung Cancer
author_sort	Huijie Duan
journal	Frontiers in Oncology
journalStr	Frontiers in Oncology
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lang_code	eng
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author_browse	Huijie Duan Zhong Lei Fei Xu Tao Pan Demin Lu Peili Ding Chunpeng Zhu Chi Pan Suzhan Zhang
container_volume	9
class	RC254-282
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author-letter	Huijie Duan
doi_str_mv	10.3389/fonc.2019.00790
author2-role	verfasserin
title_sort	park2 suppresses proliferation and tumorigenicity in non-small cell lung cancer
callnumber	RC254-282
title_auth	PARK2 Suppresses Proliferation and Tumorigenicity in Non-small Cell Lung Cancer
abstract	Aims:PARK2 mutation is originally associated with the progression of Parkinson's disease. In recent years, PARK2 has been reported as a tumor suppressor gene in various cancers, including lung cancer. However, the biological functions and potential molecular mechanisms of PARK2 in non-small cell lung cancer (NSCLC) are still unclear.Methods: The level of PARK2 expression in 32 tissue samples of NSCLC and matched non-tumor lung tissues was detected by Western blot, and 64 specimens of NSCLC tissues were detected by immunohistochemistry. H1299 and H460 cell lines were used to PARK2 overexpression models, and H460 cell line was also used to PARK2 knockdown model. Using cell viability, colony formation, cell cycle, apoptosis, migration, and invasion assay, the biological functions of PARK2 were evaluated and the potential molecular mechanism of PARK2 was investigated in vitro. Meanwhile, 22 nude mice were employed for in vivo studies.Results: Western blot analysis revealed a decrease of PARK2 protein expression in human NSCLC samples. Immunohistochemistry also identified a vastly reduced expression of PARK2 in NSCLC (72%) and low PARK2 expression was significantly associated with tumor histological grade, lymph node metastasis and advanced TNM stage. Overexpression of PARK2 suppressed cell proliferation, colony formation, migration, and invasion, arrested cell cycle progression in the G1 phase, and induced apoptosis in human non-small cell lines H1299 and H460 in vitro. Meanwhile, knockdown of PARK2 had the opposite biological functions. In addition, PARK2 significantly decreased the tumor volumes in subcutaneous xenograft model and reduced the incidence of metastatic tumors in the transfer model. Exploration of the molecular mechanism of PARK2 in NSCLC showed that PARK2 negatively regulated the EGFR/AKT/mTOR signaling pathway.Conclusions:PARK2 was an important tumor suppressor in NSCLC, which might inhibit cancer growth and metastases through the down regulation of the EGFR/AKT/mTOR signaling pathway.
abstractGer	Aims:PARK2 mutation is originally associated with the progression of Parkinson's disease. In recent years, PARK2 has been reported as a tumor suppressor gene in various cancers, including lung cancer. However, the biological functions and potential molecular mechanisms of PARK2 in non-small cell lung cancer (NSCLC) are still unclear.Methods: The level of PARK2 expression in 32 tissue samples of NSCLC and matched non-tumor lung tissues was detected by Western blot, and 64 specimens of NSCLC tissues were detected by immunohistochemistry. H1299 and H460 cell lines were used to PARK2 overexpression models, and H460 cell line was also used to PARK2 knockdown model. Using cell viability, colony formation, cell cycle, apoptosis, migration, and invasion assay, the biological functions of PARK2 were evaluated and the potential molecular mechanism of PARK2 was investigated in vitro. Meanwhile, 22 nude mice were employed for in vivo studies.Results: Western blot analysis revealed a decrease of PARK2 protein expression in human NSCLC samples. Immunohistochemistry also identified a vastly reduced expression of PARK2 in NSCLC (72%) and low PARK2 expression was significantly associated with tumor histological grade, lymph node metastasis and advanced TNM stage. Overexpression of PARK2 suppressed cell proliferation, colony formation, migration, and invasion, arrested cell cycle progression in the G1 phase, and induced apoptosis in human non-small cell lines H1299 and H460 in vitro. Meanwhile, knockdown of PARK2 had the opposite biological functions. In addition, PARK2 significantly decreased the tumor volumes in subcutaneous xenograft model and reduced the incidence of metastatic tumors in the transfer model. Exploration of the molecular mechanism of PARK2 in NSCLC showed that PARK2 negatively regulated the EGFR/AKT/mTOR signaling pathway.Conclusions:PARK2 was an important tumor suppressor in NSCLC, which might inhibit cancer growth and metastases through the down regulation of the EGFR/AKT/mTOR signaling pathway.
abstract_unstemmed	Aims:PARK2 mutation is originally associated with the progression of Parkinson's disease. In recent years, PARK2 has been reported as a tumor suppressor gene in various cancers, including lung cancer. However, the biological functions and potential molecular mechanisms of PARK2 in non-small cell lung cancer (NSCLC) are still unclear.Methods: The level of PARK2 expression in 32 tissue samples of NSCLC and matched non-tumor lung tissues was detected by Western blot, and 64 specimens of NSCLC tissues were detected by immunohistochemistry. H1299 and H460 cell lines were used to PARK2 overexpression models, and H460 cell line was also used to PARK2 knockdown model. Using cell viability, colony formation, cell cycle, apoptosis, migration, and invasion assay, the biological functions of PARK2 were evaluated and the potential molecular mechanism of PARK2 was investigated in vitro. Meanwhile, 22 nude mice were employed for in vivo studies.Results: Western blot analysis revealed a decrease of PARK2 protein expression in human NSCLC samples. Immunohistochemistry also identified a vastly reduced expression of PARK2 in NSCLC (72%) and low PARK2 expression was significantly associated with tumor histological grade, lymph node metastasis and advanced TNM stage. Overexpression of PARK2 suppressed cell proliferation, colony formation, migration, and invasion, arrested cell cycle progression in the G1 phase, and induced apoptosis in human non-small cell lines H1299 and H460 in vitro. Meanwhile, knockdown of PARK2 had the opposite biological functions. In addition, PARK2 significantly decreased the tumor volumes in subcutaneous xenograft model and reduced the incidence of metastatic tumors in the transfer model. Exploration of the molecular mechanism of PARK2 in NSCLC showed that PARK2 negatively regulated the EGFR/AKT/mTOR signaling pathway.Conclusions:PARK2 was an important tumor suppressor in NSCLC, which might inhibit cancer growth and metastases through the down regulation of the EGFR/AKT/mTOR signaling pathway.
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title_short	PARK2 Suppresses Proliferation and Tumorigenicity in Non-small Cell Lung Cancer
url	https://doi.org/10.3389/fonc.2019.00790 https://doaj.org/article/574a1e058b4d4f7bbc455032b4ff3a0b https://www.frontiersin.org/article/10.3389/fonc.2019.00790/full https://doaj.org/toc/2234-943X
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author2	Huijie Duan Zhong Lei Fei Xu Tao Pan Demin Lu Peili Ding Chunpeng Zhu Chi Pan Suzhan Zhang
author2Str	Huijie Duan Zhong Lei Fei Xu Tao Pan Demin Lu Peili Ding Chunpeng Zhu Chi Pan Suzhan Zhang
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up_date	2024-07-04T01:03:20.538Z
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