Downregulation of NSD3 (WHSC1L1) inhibits cell proliferation and migration via ERK1/2 deactivation and decreasing CAPG expression in colorectal cancer cells

Lanjuan Yi,1 Lanjie Yi,2 Qing Liu,3 Chen Li41Department of gastroenterology, Yantai Shan Hospital, Yantai, Shandong 264001, People’s Republic of China; 2Research Office of Clinical literature, Nanjing University of Chinese Medicine, Nanjing, Jiangsu 210023, People’s Republic of China; 3Department of Nosocomial Infection Control, Xuzhou Hospital of Traditional Chinese Medicine Affiliated to Nanjing University of Chinese Medicine, Xuzhou, Jiangsu 310015, People’s Republic of China; 4Department of Gastroenterology, Xuzhou Chinese Medicine Hospital Affiliated to Nanjing University of Chinese Medicine, Xuzhou, Jiangsu 310015, People’s Republic of ChinaPurpose: NSD3 (WHSC1L1) is a protein lysine methyltransferase that is recurrently amplified (8p11.23) in several cancer types, and its upregulation is involved in tumor cell proliferation, metastasis, and epithelial-mesenchymal transition (EMT). We aimed to evaluate its potential function as an oncogenic force in colorectal cancer (CRC), and to elucidate relevant mechanisms of its oncogenic activity.Materials and methods: NSD3 levels were analyzed in human CRC and adjacent normal tissues or cells by Western blot analysis and RT-qPCR. Expression levels of the proteins were detected by Western blot analysis and RT-qPCR.Results: NSD3 was significantly upregulated in both CRC tissues and cell lines. Knockdown of NSD3 expression resulted in significant decreases in CRC cell proliferation, migration, and EMT process marker proteins vimentin, simultaneously reducing E-cadherin and N-cadherin expression. The opposite results were observed when NSD3 was overexpressed. Additionally, overexpressing of NSD3 dramatically activated the extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathway and enhanced actin-capping protein (CAPG) expression. Furthermore, the proliferation and migration abilities evidently facilitated by pcDNA3.1(+) expression vector containing full-length CDS of NSD3 (pcDNA3.1(+)-NSD3, or NSD3) were partially decreased after incubation with ERK1/2 signaling pathway inhibitor (PD98059) and/or specific siRNA against CAPG (siCAPG) in SW480 and HT-29 CRC cells.Conclusion: NSD3 overexpression stimulated CRC cell proliferation and migration through targeting the ERK1/2 signaling pathway and downstream CAPG. Thus, NSD3 could serve as a promising target for anticancer drug development for patients with CRC.Keywords: colorectal cancer, histone methyltransferase NSD3, extracellular signal-regulated kinase 1/2, actin-capping protein (CAPG) Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Yi L [verfasserIn] Liu Q [verfasserIn] Li C [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2019

Schlagwörter:	colorectal cancer histone methyltransferase NSD3 extracellular signal-regulated kinase 1/2 actin-capping protein (CAPG)

Übergeordnetes Werk:	In: OncoTargets and Therapy - Dove Medical Press, 2009, (2019), Seite 3933-3943
Übergeordnetes Werk:	year:2019 ; pages:3933-3943

Links:	Link aufrufen Link aufrufen Journal toc

Katalog-ID:	DOAJ040205878

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520			\|a Lanjuan Yi,1 Lanjie Yi,2 Qing Liu,3 Chen Li41Department of gastroenterology, Yantai Shan Hospital, Yantai, Shandong 264001, People’s Republic of China; 2Research Office of Clinical literature, Nanjing University of Chinese Medicine, Nanjing, Jiangsu 210023, People’s Republic of China; 3Department of Nosocomial Infection Control, Xuzhou Hospital of Traditional Chinese Medicine Affiliated to Nanjing University of Chinese Medicine, Xuzhou, Jiangsu 310015, People’s Republic of China; 4Department of Gastroenterology, Xuzhou Chinese Medicine Hospital Affiliated to Nanjing University of Chinese Medicine, Xuzhou, Jiangsu 310015, People’s Republic of ChinaPurpose: NSD3 (WHSC1L1) is a protein lysine methyltransferase that is recurrently amplified (8p11.23) in several cancer types, and its upregulation is involved in tumor cell proliferation, metastasis, and epithelial-mesenchymal transition (EMT). We aimed to evaluate its potential function as an oncogenic force in colorectal cancer (CRC), and to elucidate relevant mechanisms of its oncogenic activity.Materials and methods: NSD3 levels were analyzed in human CRC and adjacent normal tissues or cells by Western blot analysis and RT-qPCR. Expression levels of the proteins were detected by Western blot analysis and RT-qPCR.Results: NSD3 was significantly upregulated in both CRC tissues and cell lines. Knockdown of NSD3 expression resulted in significant decreases in CRC cell proliferation, migration, and EMT process marker proteins vimentin, simultaneously reducing E-cadherin and N-cadherin expression. The opposite results were observed when NSD3 was overexpressed. Additionally, overexpressing of NSD3 dramatically activated the extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathway and enhanced actin-capping protein (CAPG) expression. Furthermore, the proliferation and migration abilities evidently facilitated by pcDNA3.1(+) expression vector containing full-length CDS of NSD3 (pcDNA3.1(+)-NSD3, or NSD3) were partially decreased after incubation with ERK1/2 signaling pathway inhibitor (PD98059) and/or specific siRNA against CAPG (siCAPG) in SW480 and HT-29 CRC cells.Conclusion: NSD3 overexpression stimulated CRC cell proliferation and migration through targeting the ERK1/2 signaling pathway and downstream CAPG. Thus, NSD3 could serve as a promising target for anticancer drug development for patients with CRC.Keywords: colorectal cancer, histone methyltransferase NSD3, extracellular signal-regulated kinase 1/2, actin-capping protein (CAPG)
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allfields	(DE-627)DOAJ040205878 (DE-599)DOAJ180e5503ca40400896ba632f55a3958d DE-627 ger DE-627 rakwb eng RC254-282 Yi L verfasserin aut Downregulation of NSD3 (WHSC1L1) inhibits cell proliferation and migration via ERK1/2 deactivation and decreasing CAPG expression in colorectal cancer cells 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Lanjuan Yi,1 Lanjie Yi,2 Qing Liu,3 Chen Li41Department of gastroenterology, Yantai Shan Hospital, Yantai, Shandong 264001, People’s Republic of China; 2Research Office of Clinical literature, Nanjing University of Chinese Medicine, Nanjing, Jiangsu 210023, People’s Republic of China; 3Department of Nosocomial Infection Control, Xuzhou Hospital of Traditional Chinese Medicine Affiliated to Nanjing University of Chinese Medicine, Xuzhou, Jiangsu 310015, People’s Republic of China; 4Department of Gastroenterology, Xuzhou Chinese Medicine Hospital Affiliated to Nanjing University of Chinese Medicine, Xuzhou, Jiangsu 310015, People’s Republic of ChinaPurpose: NSD3 (WHSC1L1) is a protein lysine methyltransferase that is recurrently amplified (8p11.23) in several cancer types, and its upregulation is involved in tumor cell proliferation, metastasis, and epithelial-mesenchymal transition (EMT). We aimed to evaluate its potential function as an oncogenic force in colorectal cancer (CRC), and to elucidate relevant mechanisms of its oncogenic activity.Materials and methods: NSD3 levels were analyzed in human CRC and adjacent normal tissues or cells by Western blot analysis and RT-qPCR. Expression levels of the proteins were detected by Western blot analysis and RT-qPCR.Results: NSD3 was significantly upregulated in both CRC tissues and cell lines. Knockdown of NSD3 expression resulted in significant decreases in CRC cell proliferation, migration, and EMT process marker proteins vimentin, simultaneously reducing E-cadherin and N-cadherin expression. The opposite results were observed when NSD3 was overexpressed. Additionally, overexpressing of NSD3 dramatically activated the extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathway and enhanced actin-capping protein (CAPG) expression. Furthermore, the proliferation and migration abilities evidently facilitated by pcDNA3.1(+) expression vector containing full-length CDS of NSD3 (pcDNA3.1(+)-NSD3, or NSD3) were partially decreased after incubation with ERK1/2 signaling pathway inhibitor (PD98059) and/or specific siRNA against CAPG (siCAPG) in SW480 and HT-29 CRC cells.Conclusion: NSD3 overexpression stimulated CRC cell proliferation and migration through targeting the ERK1/2 signaling pathway and downstream CAPG. Thus, NSD3 could serve as a promising target for anticancer drug development for patients with CRC.Keywords: colorectal cancer, histone methyltransferase NSD3, extracellular signal-regulated kinase 1/2, actin-capping protein (CAPG) colorectal cancer histone methyltransferase NSD3 extracellular signal-regulated kinase 1/2 actin-capping protein (CAPG) Neoplasms. Tumors. Oncology. Including cancer and carcinogens Yi L verfasserin aut Liu Q verfasserin aut Li C verfasserin aut In OncoTargets and Therapy Dove Medical Press, 2009 (2019), Seite 3933-3943 (DE-627)600307654 (DE-600)2495130-4 11786930 nnns year:2019 pages:3933-3943 https://doaj.org/article/180e5503ca40400896ba632f55a3958d kostenfrei https://www.dovepress.com/downregulation-of-nsd3-whsc1l1-inhibits-cell-proliferation-and-migrati-peer-reviewed-article-OTT kostenfrei https://doaj.org/toc/1178-6930 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_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 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 2019 3933-3943
spelling	(DE-627)DOAJ040205878 (DE-599)DOAJ180e5503ca40400896ba632f55a3958d DE-627 ger DE-627 rakwb eng RC254-282 Yi L verfasserin aut Downregulation of NSD3 (WHSC1L1) inhibits cell proliferation and migration via ERK1/2 deactivation and decreasing CAPG expression in colorectal cancer cells 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Lanjuan Yi,1 Lanjie Yi,2 Qing Liu,3 Chen Li41Department of gastroenterology, Yantai Shan Hospital, Yantai, Shandong 264001, People’s Republic of China; 2Research Office of Clinical literature, Nanjing University of Chinese Medicine, Nanjing, Jiangsu 210023, People’s Republic of China; 3Department of Nosocomial Infection Control, Xuzhou Hospital of Traditional Chinese Medicine Affiliated to Nanjing University of Chinese Medicine, Xuzhou, Jiangsu 310015, People’s Republic of China; 4Department of Gastroenterology, Xuzhou Chinese Medicine Hospital Affiliated to Nanjing University of Chinese Medicine, Xuzhou, Jiangsu 310015, People’s Republic of ChinaPurpose: NSD3 (WHSC1L1) is a protein lysine methyltransferase that is recurrently amplified (8p11.23) in several cancer types, and its upregulation is involved in tumor cell proliferation, metastasis, and epithelial-mesenchymal transition (EMT). We aimed to evaluate its potential function as an oncogenic force in colorectal cancer (CRC), and to elucidate relevant mechanisms of its oncogenic activity.Materials and methods: NSD3 levels were analyzed in human CRC and adjacent normal tissues or cells by Western blot analysis and RT-qPCR. Expression levels of the proteins were detected by Western blot analysis and RT-qPCR.Results: NSD3 was significantly upregulated in both CRC tissues and cell lines. Knockdown of NSD3 expression resulted in significant decreases in CRC cell proliferation, migration, and EMT process marker proteins vimentin, simultaneously reducing E-cadherin and N-cadherin expression. The opposite results were observed when NSD3 was overexpressed. Additionally, overexpressing of NSD3 dramatically activated the extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathway and enhanced actin-capping protein (CAPG) expression. Furthermore, the proliferation and migration abilities evidently facilitated by pcDNA3.1(+) expression vector containing full-length CDS of NSD3 (pcDNA3.1(+)-NSD3, or NSD3) were partially decreased after incubation with ERK1/2 signaling pathway inhibitor (PD98059) and/or specific siRNA against CAPG (siCAPG) in SW480 and HT-29 CRC cells.Conclusion: NSD3 overexpression stimulated CRC cell proliferation and migration through targeting the ERK1/2 signaling pathway and downstream CAPG. Thus, NSD3 could serve as a promising target for anticancer drug development for patients with CRC.Keywords: colorectal cancer, histone methyltransferase NSD3, extracellular signal-regulated kinase 1/2, actin-capping protein (CAPG) colorectal cancer histone methyltransferase NSD3 extracellular signal-regulated kinase 1/2 actin-capping protein (CAPG) Neoplasms. Tumors. Oncology. Including cancer and carcinogens Yi L verfasserin aut Liu Q verfasserin aut Li C verfasserin aut In OncoTargets and Therapy Dove Medical Press, 2009 (2019), Seite 3933-3943 (DE-627)600307654 (DE-600)2495130-4 11786930 nnns year:2019 pages:3933-3943 https://doaj.org/article/180e5503ca40400896ba632f55a3958d kostenfrei https://www.dovepress.com/downregulation-of-nsd3-whsc1l1-inhibits-cell-proliferation-and-migrati-peer-reviewed-article-OTT kostenfrei https://doaj.org/toc/1178-6930 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_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 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 2019 3933-3943
allfields_unstemmed	(DE-627)DOAJ040205878 (DE-599)DOAJ180e5503ca40400896ba632f55a3958d DE-627 ger DE-627 rakwb eng RC254-282 Yi L verfasserin aut Downregulation of NSD3 (WHSC1L1) inhibits cell proliferation and migration via ERK1/2 deactivation and decreasing CAPG expression in colorectal cancer cells 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Lanjuan Yi,1 Lanjie Yi,2 Qing Liu,3 Chen Li41Department of gastroenterology, Yantai Shan Hospital, Yantai, Shandong 264001, People’s Republic of China; 2Research Office of Clinical literature, Nanjing University of Chinese Medicine, Nanjing, Jiangsu 210023, People’s Republic of China; 3Department of Nosocomial Infection Control, Xuzhou Hospital of Traditional Chinese Medicine Affiliated to Nanjing University of Chinese Medicine, Xuzhou, Jiangsu 310015, People’s Republic of China; 4Department of Gastroenterology, Xuzhou Chinese Medicine Hospital Affiliated to Nanjing University of Chinese Medicine, Xuzhou, Jiangsu 310015, People’s Republic of ChinaPurpose: NSD3 (WHSC1L1) is a protein lysine methyltransferase that is recurrently amplified (8p11.23) in several cancer types, and its upregulation is involved in tumor cell proliferation, metastasis, and epithelial-mesenchymal transition (EMT). We aimed to evaluate its potential function as an oncogenic force in colorectal cancer (CRC), and to elucidate relevant mechanisms of its oncogenic activity.Materials and methods: NSD3 levels were analyzed in human CRC and adjacent normal tissues or cells by Western blot analysis and RT-qPCR. Expression levels of the proteins were detected by Western blot analysis and RT-qPCR.Results: NSD3 was significantly upregulated in both CRC tissues and cell lines. Knockdown of NSD3 expression resulted in significant decreases in CRC cell proliferation, migration, and EMT process marker proteins vimentin, simultaneously reducing E-cadherin and N-cadherin expression. The opposite results were observed when NSD3 was overexpressed. Additionally, overexpressing of NSD3 dramatically activated the extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathway and enhanced actin-capping protein (CAPG) expression. Furthermore, the proliferation and migration abilities evidently facilitated by pcDNA3.1(+) expression vector containing full-length CDS of NSD3 (pcDNA3.1(+)-NSD3, or NSD3) were partially decreased after incubation with ERK1/2 signaling pathway inhibitor (PD98059) and/or specific siRNA against CAPG (siCAPG) in SW480 and HT-29 CRC cells.Conclusion: NSD3 overexpression stimulated CRC cell proliferation and migration through targeting the ERK1/2 signaling pathway and downstream CAPG. Thus, NSD3 could serve as a promising target for anticancer drug development for patients with CRC.Keywords: colorectal cancer, histone methyltransferase NSD3, extracellular signal-regulated kinase 1/2, actin-capping protein (CAPG) colorectal cancer histone methyltransferase NSD3 extracellular signal-regulated kinase 1/2 actin-capping protein (CAPG) Neoplasms. Tumors. Oncology. Including cancer and carcinogens Yi L verfasserin aut Liu Q verfasserin aut Li C verfasserin aut In OncoTargets and Therapy Dove Medical Press, 2009 (2019), Seite 3933-3943 (DE-627)600307654 (DE-600)2495130-4 11786930 nnns year:2019 pages:3933-3943 https://doaj.org/article/180e5503ca40400896ba632f55a3958d kostenfrei https://www.dovepress.com/downregulation-of-nsd3-whsc1l1-inhibits-cell-proliferation-and-migrati-peer-reviewed-article-OTT kostenfrei https://doaj.org/toc/1178-6930 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_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 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 2019 3933-3943
allfieldsGer	(DE-627)DOAJ040205878 (DE-599)DOAJ180e5503ca40400896ba632f55a3958d DE-627 ger DE-627 rakwb eng RC254-282 Yi L verfasserin aut Downregulation of NSD3 (WHSC1L1) inhibits cell proliferation and migration via ERK1/2 deactivation and decreasing CAPG expression in colorectal cancer cells 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Lanjuan Yi,1 Lanjie Yi,2 Qing Liu,3 Chen Li41Department of gastroenterology, Yantai Shan Hospital, Yantai, Shandong 264001, People’s Republic of China; 2Research Office of Clinical literature, Nanjing University of Chinese Medicine, Nanjing, Jiangsu 210023, People’s Republic of China; 3Department of Nosocomial Infection Control, Xuzhou Hospital of Traditional Chinese Medicine Affiliated to Nanjing University of Chinese Medicine, Xuzhou, Jiangsu 310015, People’s Republic of China; 4Department of Gastroenterology, Xuzhou Chinese Medicine Hospital Affiliated to Nanjing University of Chinese Medicine, Xuzhou, Jiangsu 310015, People’s Republic of ChinaPurpose: NSD3 (WHSC1L1) is a protein lysine methyltransferase that is recurrently amplified (8p11.23) in several cancer types, and its upregulation is involved in tumor cell proliferation, metastasis, and epithelial-mesenchymal transition (EMT). We aimed to evaluate its potential function as an oncogenic force in colorectal cancer (CRC), and to elucidate relevant mechanisms of its oncogenic activity.Materials and methods: NSD3 levels were analyzed in human CRC and adjacent normal tissues or cells by Western blot analysis and RT-qPCR. Expression levels of the proteins were detected by Western blot analysis and RT-qPCR.Results: NSD3 was significantly upregulated in both CRC tissues and cell lines. Knockdown of NSD3 expression resulted in significant decreases in CRC cell proliferation, migration, and EMT process marker proteins vimentin, simultaneously reducing E-cadherin and N-cadherin expression. The opposite results were observed when NSD3 was overexpressed. Additionally, overexpressing of NSD3 dramatically activated the extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathway and enhanced actin-capping protein (CAPG) expression. Furthermore, the proliferation and migration abilities evidently facilitated by pcDNA3.1(+) expression vector containing full-length CDS of NSD3 (pcDNA3.1(+)-NSD3, or NSD3) were partially decreased after incubation with ERK1/2 signaling pathway inhibitor (PD98059) and/or specific siRNA against CAPG (siCAPG) in SW480 and HT-29 CRC cells.Conclusion: NSD3 overexpression stimulated CRC cell proliferation and migration through targeting the ERK1/2 signaling pathway and downstream CAPG. Thus, NSD3 could serve as a promising target for anticancer drug development for patients with CRC.Keywords: colorectal cancer, histone methyltransferase NSD3, extracellular signal-regulated kinase 1/2, actin-capping protein (CAPG) colorectal cancer histone methyltransferase NSD3 extracellular signal-regulated kinase 1/2 actin-capping protein (CAPG) Neoplasms. Tumors. Oncology. Including cancer and carcinogens Yi L verfasserin aut Liu Q verfasserin aut Li C verfasserin aut In OncoTargets and Therapy Dove Medical Press, 2009 (2019), Seite 3933-3943 (DE-627)600307654 (DE-600)2495130-4 11786930 nnns year:2019 pages:3933-3943 https://doaj.org/article/180e5503ca40400896ba632f55a3958d kostenfrei https://www.dovepress.com/downregulation-of-nsd3-whsc1l1-inhibits-cell-proliferation-and-migrati-peer-reviewed-article-OTT kostenfrei https://doaj.org/toc/1178-6930 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_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 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 2019 3933-3943
allfieldsSound	(DE-627)DOAJ040205878 (DE-599)DOAJ180e5503ca40400896ba632f55a3958d DE-627 ger DE-627 rakwb eng RC254-282 Yi L verfasserin aut Downregulation of NSD3 (WHSC1L1) inhibits cell proliferation and migration via ERK1/2 deactivation and decreasing CAPG expression in colorectal cancer cells 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Lanjuan Yi,1 Lanjie Yi,2 Qing Liu,3 Chen Li41Department of gastroenterology, Yantai Shan Hospital, Yantai, Shandong 264001, People’s Republic of China; 2Research Office of Clinical literature, Nanjing University of Chinese Medicine, Nanjing, Jiangsu 210023, People’s Republic of China; 3Department of Nosocomial Infection Control, Xuzhou Hospital of Traditional Chinese Medicine Affiliated to Nanjing University of Chinese Medicine, Xuzhou, Jiangsu 310015, People’s Republic of China; 4Department of Gastroenterology, Xuzhou Chinese Medicine Hospital Affiliated to Nanjing University of Chinese Medicine, Xuzhou, Jiangsu 310015, People’s Republic of ChinaPurpose: NSD3 (WHSC1L1) is a protein lysine methyltransferase that is recurrently amplified (8p11.23) in several cancer types, and its upregulation is involved in tumor cell proliferation, metastasis, and epithelial-mesenchymal transition (EMT). We aimed to evaluate its potential function as an oncogenic force in colorectal cancer (CRC), and to elucidate relevant mechanisms of its oncogenic activity.Materials and methods: NSD3 levels were analyzed in human CRC and adjacent normal tissues or cells by Western blot analysis and RT-qPCR. Expression levels of the proteins were detected by Western blot analysis and RT-qPCR.Results: NSD3 was significantly upregulated in both CRC tissues and cell lines. Knockdown of NSD3 expression resulted in significant decreases in CRC cell proliferation, migration, and EMT process marker proteins vimentin, simultaneously reducing E-cadherin and N-cadherin expression. The opposite results were observed when NSD3 was overexpressed. Additionally, overexpressing of NSD3 dramatically activated the extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathway and enhanced actin-capping protein (CAPG) expression. Furthermore, the proliferation and migration abilities evidently facilitated by pcDNA3.1(+) expression vector containing full-length CDS of NSD3 (pcDNA3.1(+)-NSD3, or NSD3) were partially decreased after incubation with ERK1/2 signaling pathway inhibitor (PD98059) and/or specific siRNA against CAPG (siCAPG) in SW480 and HT-29 CRC cells.Conclusion: NSD3 overexpression stimulated CRC cell proliferation and migration through targeting the ERK1/2 signaling pathway and downstream CAPG. Thus, NSD3 could serve as a promising target for anticancer drug development for patients with CRC.Keywords: colorectal cancer, histone methyltransferase NSD3, extracellular signal-regulated kinase 1/2, actin-capping protein (CAPG) colorectal cancer histone methyltransferase NSD3 extracellular signal-regulated kinase 1/2 actin-capping protein (CAPG) Neoplasms. Tumors. Oncology. Including cancer and carcinogens Yi L verfasserin aut Liu Q verfasserin aut Li C verfasserin aut In OncoTargets and Therapy Dove Medical Press, 2009 (2019), Seite 3933-3943 (DE-627)600307654 (DE-600)2495130-4 11786930 nnns year:2019 pages:3933-3943 https://doaj.org/article/180e5503ca40400896ba632f55a3958d kostenfrei https://www.dovepress.com/downregulation-of-nsd3-whsc1l1-inhibits-cell-proliferation-and-migrati-peer-reviewed-article-OTT kostenfrei https://doaj.org/toc/1178-6930 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_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 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 2019 3933-3943
language	English
source	In OncoTargets and Therapy (2019), Seite 3933-3943 year:2019 pages:3933-3943
sourceStr	In OncoTargets and Therapy (2019), Seite 3933-3943 year:2019 pages:3933-3943
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	colorectal cancer histone methyltransferase NSD3 extracellular signal-regulated kinase 1/2 actin-capping protein (CAPG) Neoplasms. Tumors. Oncology. Including cancer and carcinogens
isfreeaccess_bool	true
container_title	OncoTargets and Therapy
authorswithroles_txt_mv	Yi L @@aut@@ Liu Q @@aut@@ Li C @@aut@@
publishDateDaySort_date	2019-01-01T00:00:00Z
hierarchy_top_id	600307654
id	DOAJ040205878
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">DOAJ040205878</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230308034434.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">230227s2019 xx \|\|\|\|\|o 00\| \|\|eng c</controlfield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)DOAJ040205878</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)DOAJ180e5503ca40400896ba632f55a3958d</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">RC254-282</subfield></datafield><datafield tag="100" ind1="0" ind2=" "><subfield code="a">Yi L</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Downregulation of NSD3 (WHSC1L1) inhibits cell proliferation and migration via ERK1/2 deactivation and decreasing CAPG expression in colorectal cancer cells</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2019</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">Lanjuan Yi,1 Lanjie Yi,2 Qing Liu,3 Chen Li41Department of gastroenterology, Yantai Shan Hospital, Yantai, Shandong 264001, People&rsquo;s Republic of China; 2Research Office of Clinical literature, Nanjing University of Chinese Medicine, Nanjing, Jiangsu 210023, People&rsquo;s Republic of China; 3Department of Nosocomial Infection Control, Xuzhou Hospital of Traditional Chinese Medicine Affiliated to Nanjing University of Chinese Medicine, Xuzhou, Jiangsu 310015, People&rsquo;s Republic of China; 4Department of Gastroenterology, Xuzhou Chinese Medicine Hospital Affiliated to Nanjing University of Chinese Medicine, Xuzhou, Jiangsu 310015, People&rsquo;s Republic of ChinaPurpose: NSD3 (WHSC1L1) is a protein lysine methyltransferase that is recurrently amplified (8p11.23) in several cancer types, and its upregulation is involved in tumor cell proliferation, metastasis, and epithelial-mesenchymal transition (EMT). We aimed to evaluate its potential function as an oncogenic force in colorectal cancer (CRC), and to elucidate relevant mechanisms of its oncogenic activity.Materials and methods: NSD3 levels were analyzed in human CRC and adjacent normal tissues or cells by Western blot analysis and RT-qPCR. Expression levels of the proteins were detected by Western blot analysis and RT-qPCR.Results: NSD3 was significantly upregulated in both CRC tissues and cell lines. Knockdown of NSD3 expression resulted in significant decreases in CRC cell proliferation, migration, and EMT process marker proteins vimentin, simultaneously reducing E-cadherin and N-cadherin expression. The opposite results were observed when NSD3 was overexpressed. Additionally, overexpressing of NSD3 dramatically activated the extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathway and enhanced actin-capping protein (CAPG) expression. Furthermore, the proliferation and migration abilities evidently facilitated by pcDNA3.1(+) expression vector containing full-length CDS of NSD3 (pcDNA3.1(+)-NSD3, or NSD3) were partially decreased after incubation with ERK1/2 signaling pathway inhibitor (PD98059) and/or specific siRNA against CAPG (siCAPG) in SW480 and HT-29 CRC cells.Conclusion: NSD3 overexpression stimulated CRC cell proliferation and migration through targeting the ERK1/2 signaling pathway and downstream CAPG. 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callnumber-first	R - Medicine
author	Yi L
spellingShingle	Yi L misc RC254-282 misc colorectal cancer misc histone methyltransferase NSD3 misc extracellular signal-regulated kinase 1/2 misc actin-capping protein (CAPG) misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens Downregulation of NSD3 (WHSC1L1) inhibits cell proliferation and migration via ERK1/2 deactivation and decreasing CAPG expression in colorectal cancer cells
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topic_title	RC254-282 Downregulation of NSD3 (WHSC1L1) inhibits cell proliferation and migration via ERK1/2 deactivation and decreasing CAPG expression in colorectal cancer cells colorectal cancer histone methyltransferase NSD3 extracellular signal-regulated kinase 1/2 actin-capping protein (CAPG)
topic	misc RC254-282 misc colorectal cancer misc histone methyltransferase NSD3 misc extracellular signal-regulated kinase 1/2 misc actin-capping protein (CAPG) misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens
topic_unstemmed	misc RC254-282 misc colorectal cancer misc histone methyltransferase NSD3 misc extracellular signal-regulated kinase 1/2 misc actin-capping protein (CAPG) misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens
topic_browse	misc RC254-282 misc colorectal cancer misc histone methyltransferase NSD3 misc extracellular signal-regulated kinase 1/2 misc actin-capping protein (CAPG) misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens
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title	Downregulation of NSD3 (WHSC1L1) inhibits cell proliferation and migration via ERK1/2 deactivation and decreasing CAPG expression in colorectal cancer cells
ctrlnum	(DE-627)DOAJ040205878 (DE-599)DOAJ180e5503ca40400896ba632f55a3958d
title_full	Downregulation of NSD3 (WHSC1L1) inhibits cell proliferation and migration via ERK1/2 deactivation and decreasing CAPG expression in colorectal cancer cells
author_sort	Yi L
journal	OncoTargets and Therapy
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title_sort	downregulation of nsd3 (whsc1l1) inhibits cell proliferation and migration via erk1/2 deactivation and decreasing capg expression in colorectal cancer cells
callnumber	RC254-282
title_auth	Downregulation of NSD3 (WHSC1L1) inhibits cell proliferation and migration via ERK1/2 deactivation and decreasing CAPG expression in colorectal cancer cells
abstract	Lanjuan Yi,1 Lanjie Yi,2 Qing Liu,3 Chen Li41Department of gastroenterology, Yantai Shan Hospital, Yantai, Shandong 264001, People’s Republic of China; 2Research Office of Clinical literature, Nanjing University of Chinese Medicine, Nanjing, Jiangsu 210023, People’s Republic of China; 3Department of Nosocomial Infection Control, Xuzhou Hospital of Traditional Chinese Medicine Affiliated to Nanjing University of Chinese Medicine, Xuzhou, Jiangsu 310015, People’s Republic of China; 4Department of Gastroenterology, Xuzhou Chinese Medicine Hospital Affiliated to Nanjing University of Chinese Medicine, Xuzhou, Jiangsu 310015, People’s Republic of ChinaPurpose: NSD3 (WHSC1L1) is a protein lysine methyltransferase that is recurrently amplified (8p11.23) in several cancer types, and its upregulation is involved in tumor cell proliferation, metastasis, and epithelial-mesenchymal transition (EMT). We aimed to evaluate its potential function as an oncogenic force in colorectal cancer (CRC), and to elucidate relevant mechanisms of its oncogenic activity.Materials and methods: NSD3 levels were analyzed in human CRC and adjacent normal tissues or cells by Western blot analysis and RT-qPCR. Expression levels of the proteins were detected by Western blot analysis and RT-qPCR.Results: NSD3 was significantly upregulated in both CRC tissues and cell lines. Knockdown of NSD3 expression resulted in significant decreases in CRC cell proliferation, migration, and EMT process marker proteins vimentin, simultaneously reducing E-cadherin and N-cadherin expression. The opposite results were observed when NSD3 was overexpressed. Additionally, overexpressing of NSD3 dramatically activated the extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathway and enhanced actin-capping protein (CAPG) expression. Furthermore, the proliferation and migration abilities evidently facilitated by pcDNA3.1(+) expression vector containing full-length CDS of NSD3 (pcDNA3.1(+)-NSD3, or NSD3) were partially decreased after incubation with ERK1/2 signaling pathway inhibitor (PD98059) and/or specific siRNA against CAPG (siCAPG) in SW480 and HT-29 CRC cells.Conclusion: NSD3 overexpression stimulated CRC cell proliferation and migration through targeting the ERK1/2 signaling pathway and downstream CAPG. Thus, NSD3 could serve as a promising target for anticancer drug development for patients with CRC.Keywords: colorectal cancer, histone methyltransferase NSD3, extracellular signal-regulated kinase 1/2, actin-capping protein (CAPG)
abstractGer	Lanjuan Yi,1 Lanjie Yi,2 Qing Liu,3 Chen Li41Department of gastroenterology, Yantai Shan Hospital, Yantai, Shandong 264001, People’s Republic of China; 2Research Office of Clinical literature, Nanjing University of Chinese Medicine, Nanjing, Jiangsu 210023, People’s Republic of China; 3Department of Nosocomial Infection Control, Xuzhou Hospital of Traditional Chinese Medicine Affiliated to Nanjing University of Chinese Medicine, Xuzhou, Jiangsu 310015, People’s Republic of China; 4Department of Gastroenterology, Xuzhou Chinese Medicine Hospital Affiliated to Nanjing University of Chinese Medicine, Xuzhou, Jiangsu 310015, People’s Republic of ChinaPurpose: NSD3 (WHSC1L1) is a protein lysine methyltransferase that is recurrently amplified (8p11.23) in several cancer types, and its upregulation is involved in tumor cell proliferation, metastasis, and epithelial-mesenchymal transition (EMT). We aimed to evaluate its potential function as an oncogenic force in colorectal cancer (CRC), and to elucidate relevant mechanisms of its oncogenic activity.Materials and methods: NSD3 levels were analyzed in human CRC and adjacent normal tissues or cells by Western blot analysis and RT-qPCR. Expression levels of the proteins were detected by Western blot analysis and RT-qPCR.Results: NSD3 was significantly upregulated in both CRC tissues and cell lines. Knockdown of NSD3 expression resulted in significant decreases in CRC cell proliferation, migration, and EMT process marker proteins vimentin, simultaneously reducing E-cadherin and N-cadherin expression. The opposite results were observed when NSD3 was overexpressed. Additionally, overexpressing of NSD3 dramatically activated the extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathway and enhanced actin-capping protein (CAPG) expression. Furthermore, the proliferation and migration abilities evidently facilitated by pcDNA3.1(+) expression vector containing full-length CDS of NSD3 (pcDNA3.1(+)-NSD3, or NSD3) were partially decreased after incubation with ERK1/2 signaling pathway inhibitor (PD98059) and/or specific siRNA against CAPG (siCAPG) in SW480 and HT-29 CRC cells.Conclusion: NSD3 overexpression stimulated CRC cell proliferation and migration through targeting the ERK1/2 signaling pathway and downstream CAPG. Thus, NSD3 could serve as a promising target for anticancer drug development for patients with CRC.Keywords: colorectal cancer, histone methyltransferase NSD3, extracellular signal-regulated kinase 1/2, actin-capping protein (CAPG)
abstract_unstemmed	Lanjuan Yi,1 Lanjie Yi,2 Qing Liu,3 Chen Li41Department of gastroenterology, Yantai Shan Hospital, Yantai, Shandong 264001, People’s Republic of China; 2Research Office of Clinical literature, Nanjing University of Chinese Medicine, Nanjing, Jiangsu 210023, People’s Republic of China; 3Department of Nosocomial Infection Control, Xuzhou Hospital of Traditional Chinese Medicine Affiliated to Nanjing University of Chinese Medicine, Xuzhou, Jiangsu 310015, People’s Republic of China; 4Department of Gastroenterology, Xuzhou Chinese Medicine Hospital Affiliated to Nanjing University of Chinese Medicine, Xuzhou, Jiangsu 310015, People’s Republic of ChinaPurpose: NSD3 (WHSC1L1) is a protein lysine methyltransferase that is recurrently amplified (8p11.23) in several cancer types, and its upregulation is involved in tumor cell proliferation, metastasis, and epithelial-mesenchymal transition (EMT). We aimed to evaluate its potential function as an oncogenic force in colorectal cancer (CRC), and to elucidate relevant mechanisms of its oncogenic activity.Materials and methods: NSD3 levels were analyzed in human CRC and adjacent normal tissues or cells by Western blot analysis and RT-qPCR. Expression levels of the proteins were detected by Western blot analysis and RT-qPCR.Results: NSD3 was significantly upregulated in both CRC tissues and cell lines. Knockdown of NSD3 expression resulted in significant decreases in CRC cell proliferation, migration, and EMT process marker proteins vimentin, simultaneously reducing E-cadherin and N-cadherin expression. The opposite results were observed when NSD3 was overexpressed. Additionally, overexpressing of NSD3 dramatically activated the extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathway and enhanced actin-capping protein (CAPG) expression. Furthermore, the proliferation and migration abilities evidently facilitated by pcDNA3.1(+) expression vector containing full-length CDS of NSD3 (pcDNA3.1(+)-NSD3, or NSD3) were partially decreased after incubation with ERK1/2 signaling pathway inhibitor (PD98059) and/or specific siRNA against CAPG (siCAPG) in SW480 and HT-29 CRC cells.Conclusion: NSD3 overexpression stimulated CRC cell proliferation and migration through targeting the ERK1/2 signaling pathway and downstream CAPG. Thus, NSD3 could serve as a promising target for anticancer drug development for patients with CRC.Keywords: colorectal cancer, histone methyltransferase NSD3, extracellular signal-regulated kinase 1/2, actin-capping protein (CAPG)
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title_short	Downregulation of NSD3 (WHSC1L1) inhibits cell proliferation and migration via ERK1/2 deactivation and decreasing CAPG expression in colorectal cancer cells
url	https://doaj.org/article/180e5503ca40400896ba632f55a3958d https://www.dovepress.com/downregulation-of-nsd3-whsc1l1-inhibits-cell-proliferation-and-migrati-peer-reviewed-article-OTT https://doaj.org/toc/1178-6930
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