Inhibition of integrin β3, a binding partner of kallistatin, leads to reduced viability, invasion and proliferation in NCI-H446 cells

Background Kallistatin is a serine proteinase inhibitor and heparin-binding protein. It is considered an endogenous angiogenic inhibitor. In addition, multiple studies demonstrated that kallistatin directly inhibits cancer cell growth. However, the molecular mechanisms underlying these effects remai...
Ausführliche Beschreibung

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Autor*in:	Wang, Guoquan [verfasserIn] Wang, Xiao Huang, Xiaoping Yang, Huiyong Pang, Suqiu Xie, Xiaolan Zeng, Shulan Lin, Junsheng Diao, Yong

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2016

Schlagwörter:	Focal Adhesion Kinase Small Cell Lung Cancer Cell Focal Adhesion Kinase Inhibitor Pastoris Strain GS115 Lung Cancer Cell Proliferation

Anmerkung:	© The Author(s) 2016

Übergeordnetes Werk:	Enthalten in: Cancer cell international - London : BioMed Central, 2001, 16(2016), 1 vom: 01. Dez.
Übergeordnetes Werk:	volume:16 ; year:2016 ; number:1 ; day:01 ; month:12

Links:	Volltext

DOI / URN:	10.1186/s12935-016-0365-7

Katalog-ID:	SPR028587529

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520			\|a Background Kallistatin is a serine proteinase inhibitor and heparin-binding protein. It is considered an endogenous angiogenic inhibitor. In addition, multiple studies demonstrated that kallistatin directly inhibits cancer cell growth. However, the molecular mechanisms underlying these effects remain unclear. Methods Pull-down, immunoprecipitation, and immunoblotting were used for binding experiments. To elucidate the mechanisms, integrin β3 knockdown (siRNA) or blockage (antibody treatment) on the cell surface of small the cell lung cancer NCI-H446 cell line was used. Results Interestingly, kallistatin was capable of binding integrin β3 on the cell surface of NCI-H446 cells. Meanwhile, integrin β3 knockdown or blockage resulted in loss of antitumor activities induced by kallistatin. Furthermore, kallistatin suppressed tyrosine phosphorylation of integrin β3 and its downstream signaling pathways, including FAK/-Src, AKT and Erk/MAPK. Viability, proliferation and migration of NCI-H446 cells were inhibited by kallistatin, with Bcl-2 and Grb2 downregulation, and Bax, cleaved caspase-9 and caspase 3 upregulation. Conclusions These findings reveal a novel role for kallistatin in preventing small cell lung cancer growth and mobility, by direct interaction with integrin β3, leading to blockade of the related signaling pathway.
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allfields	10.1186/s12935-016-0365-7 doi (DE-627)SPR028587529 (SPR)s12935-016-0365-7-e DE-627 ger DE-627 rakwb eng Wang, Guoquan verfasserin aut Inhibition of integrin β3, a binding partner of kallistatin, leads to reduced viability, invasion and proliferation in NCI-H446 cells 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2016 Background Kallistatin is a serine proteinase inhibitor and heparin-binding protein. It is considered an endogenous angiogenic inhibitor. In addition, multiple studies demonstrated that kallistatin directly inhibits cancer cell growth. However, the molecular mechanisms underlying these effects remain unclear. Methods Pull-down, immunoprecipitation, and immunoblotting were used for binding experiments. To elucidate the mechanisms, integrin β3 knockdown (siRNA) or blockage (antibody treatment) on the cell surface of small the cell lung cancer NCI-H446 cell line was used. Results Interestingly, kallistatin was capable of binding integrin β3 on the cell surface of NCI-H446 cells. Meanwhile, integrin β3 knockdown or blockage resulted in loss of antitumor activities induced by kallistatin. Furthermore, kallistatin suppressed tyrosine phosphorylation of integrin β3 and its downstream signaling pathways, including FAK/-Src, AKT and Erk/MAPK. Viability, proliferation and migration of NCI-H446 cells were inhibited by kallistatin, with Bcl-2 and Grb2 downregulation, and Bax, cleaved caspase-9 and caspase 3 upregulation. Conclusions These findings reveal a novel role for kallistatin in preventing small cell lung cancer growth and mobility, by direct interaction with integrin β3, leading to blockade of the related signaling pathway. Focal Adhesion Kinase (dpeaa)DE-He213 Small Cell Lung Cancer Cell (dpeaa)DE-He213 Focal Adhesion Kinase Inhibitor (dpeaa)DE-He213 Pastoris Strain GS115 (dpeaa)DE-He213 Lung Cancer Cell Proliferation (dpeaa)DE-He213 Wang, Xiao aut Huang, Xiaoping aut Yang, Huiyong aut Pang, Suqiu aut Xie, Xiaolan aut Zeng, Shulan aut Lin, Junsheng aut Diao, Yong aut Enthalten in Cancer cell international London : BioMed Central, 2001 16(2016), 1 vom: 01. Dez. (DE-627)355989204 (DE-600)2091573-1 1475-2867 nnns volume:16 year:2016 number:1 day:01 month:12 https://dx.doi.org/10.1186/s12935-016-0365-7 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 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_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 16 2016 1 01 12
spelling	10.1186/s12935-016-0365-7 doi (DE-627)SPR028587529 (SPR)s12935-016-0365-7-e DE-627 ger DE-627 rakwb eng Wang, Guoquan verfasserin aut Inhibition of integrin β3, a binding partner of kallistatin, leads to reduced viability, invasion and proliferation in NCI-H446 cells 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2016 Background Kallistatin is a serine proteinase inhibitor and heparin-binding protein. It is considered an endogenous angiogenic inhibitor. In addition, multiple studies demonstrated that kallistatin directly inhibits cancer cell growth. However, the molecular mechanisms underlying these effects remain unclear. Methods Pull-down, immunoprecipitation, and immunoblotting were used for binding experiments. To elucidate the mechanisms, integrin β3 knockdown (siRNA) or blockage (antibody treatment) on the cell surface of small the cell lung cancer NCI-H446 cell line was used. Results Interestingly, kallistatin was capable of binding integrin β3 on the cell surface of NCI-H446 cells. Meanwhile, integrin β3 knockdown or blockage resulted in loss of antitumor activities induced by kallistatin. Furthermore, kallistatin suppressed tyrosine phosphorylation of integrin β3 and its downstream signaling pathways, including FAK/-Src, AKT and Erk/MAPK. Viability, proliferation and migration of NCI-H446 cells were inhibited by kallistatin, with Bcl-2 and Grb2 downregulation, and Bax, cleaved caspase-9 and caspase 3 upregulation. Conclusions These findings reveal a novel role for kallistatin in preventing small cell lung cancer growth and mobility, by direct interaction with integrin β3, leading to blockade of the related signaling pathway. Focal Adhesion Kinase (dpeaa)DE-He213 Small Cell Lung Cancer Cell (dpeaa)DE-He213 Focal Adhesion Kinase Inhibitor (dpeaa)DE-He213 Pastoris Strain GS115 (dpeaa)DE-He213 Lung Cancer Cell Proliferation (dpeaa)DE-He213 Wang, Xiao aut Huang, Xiaoping aut Yang, Huiyong aut Pang, Suqiu aut Xie, Xiaolan aut Zeng, Shulan aut Lin, Junsheng aut Diao, Yong aut Enthalten in Cancer cell international London : BioMed Central, 2001 16(2016), 1 vom: 01. Dez. (DE-627)355989204 (DE-600)2091573-1 1475-2867 nnns volume:16 year:2016 number:1 day:01 month:12 https://dx.doi.org/10.1186/s12935-016-0365-7 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 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_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 16 2016 1 01 12
allfields_unstemmed	10.1186/s12935-016-0365-7 doi (DE-627)SPR028587529 (SPR)s12935-016-0365-7-e DE-627 ger DE-627 rakwb eng Wang, Guoquan verfasserin aut Inhibition of integrin β3, a binding partner of kallistatin, leads to reduced viability, invasion and proliferation in NCI-H446 cells 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2016 Background Kallistatin is a serine proteinase inhibitor and heparin-binding protein. It is considered an endogenous angiogenic inhibitor. In addition, multiple studies demonstrated that kallistatin directly inhibits cancer cell growth. However, the molecular mechanisms underlying these effects remain unclear. Methods Pull-down, immunoprecipitation, and immunoblotting were used for binding experiments. To elucidate the mechanisms, integrin β3 knockdown (siRNA) or blockage (antibody treatment) on the cell surface of small the cell lung cancer NCI-H446 cell line was used. Results Interestingly, kallistatin was capable of binding integrin β3 on the cell surface of NCI-H446 cells. Meanwhile, integrin β3 knockdown or blockage resulted in loss of antitumor activities induced by kallistatin. Furthermore, kallistatin suppressed tyrosine phosphorylation of integrin β3 and its downstream signaling pathways, including FAK/-Src, AKT and Erk/MAPK. Viability, proliferation and migration of NCI-H446 cells were inhibited by kallistatin, with Bcl-2 and Grb2 downregulation, and Bax, cleaved caspase-9 and caspase 3 upregulation. Conclusions These findings reveal a novel role for kallistatin in preventing small cell lung cancer growth and mobility, by direct interaction with integrin β3, leading to blockade of the related signaling pathway. Focal Adhesion Kinase (dpeaa)DE-He213 Small Cell Lung Cancer Cell (dpeaa)DE-He213 Focal Adhesion Kinase Inhibitor (dpeaa)DE-He213 Pastoris Strain GS115 (dpeaa)DE-He213 Lung Cancer Cell Proliferation (dpeaa)DE-He213 Wang, Xiao aut Huang, Xiaoping aut Yang, Huiyong aut Pang, Suqiu aut Xie, Xiaolan aut Zeng, Shulan aut Lin, Junsheng aut Diao, Yong aut Enthalten in Cancer cell international London : BioMed Central, 2001 16(2016), 1 vom: 01. Dez. (DE-627)355989204 (DE-600)2091573-1 1475-2867 nnns volume:16 year:2016 number:1 day:01 month:12 https://dx.doi.org/10.1186/s12935-016-0365-7 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 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_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 16 2016 1 01 12
allfieldsGer	10.1186/s12935-016-0365-7 doi (DE-627)SPR028587529 (SPR)s12935-016-0365-7-e DE-627 ger DE-627 rakwb eng Wang, Guoquan verfasserin aut Inhibition of integrin β3, a binding partner of kallistatin, leads to reduced viability, invasion and proliferation in NCI-H446 cells 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2016 Background Kallistatin is a serine proteinase inhibitor and heparin-binding protein. It is considered an endogenous angiogenic inhibitor. In addition, multiple studies demonstrated that kallistatin directly inhibits cancer cell growth. However, the molecular mechanisms underlying these effects remain unclear. Methods Pull-down, immunoprecipitation, and immunoblotting were used for binding experiments. To elucidate the mechanisms, integrin β3 knockdown (siRNA) or blockage (antibody treatment) on the cell surface of small the cell lung cancer NCI-H446 cell line was used. Results Interestingly, kallistatin was capable of binding integrin β3 on the cell surface of NCI-H446 cells. Meanwhile, integrin β3 knockdown or blockage resulted in loss of antitumor activities induced by kallistatin. Furthermore, kallistatin suppressed tyrosine phosphorylation of integrin β3 and its downstream signaling pathways, including FAK/-Src, AKT and Erk/MAPK. Viability, proliferation and migration of NCI-H446 cells were inhibited by kallistatin, with Bcl-2 and Grb2 downregulation, and Bax, cleaved caspase-9 and caspase 3 upregulation. Conclusions These findings reveal a novel role for kallistatin in preventing small cell lung cancer growth and mobility, by direct interaction with integrin β3, leading to blockade of the related signaling pathway. Focal Adhesion Kinase (dpeaa)DE-He213 Small Cell Lung Cancer Cell (dpeaa)DE-He213 Focal Adhesion Kinase Inhibitor (dpeaa)DE-He213 Pastoris Strain GS115 (dpeaa)DE-He213 Lung Cancer Cell Proliferation (dpeaa)DE-He213 Wang, Xiao aut Huang, Xiaoping aut Yang, Huiyong aut Pang, Suqiu aut Xie, Xiaolan aut Zeng, Shulan aut Lin, Junsheng aut Diao, Yong aut Enthalten in Cancer cell international London : BioMed Central, 2001 16(2016), 1 vom: 01. Dez. (DE-627)355989204 (DE-600)2091573-1 1475-2867 nnns volume:16 year:2016 number:1 day:01 month:12 https://dx.doi.org/10.1186/s12935-016-0365-7 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 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_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 16 2016 1 01 12
allfieldsSound	10.1186/s12935-016-0365-7 doi (DE-627)SPR028587529 (SPR)s12935-016-0365-7-e DE-627 ger DE-627 rakwb eng Wang, Guoquan verfasserin aut Inhibition of integrin β3, a binding partner of kallistatin, leads to reduced viability, invasion and proliferation in NCI-H446 cells 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2016 Background Kallistatin is a serine proteinase inhibitor and heparin-binding protein. It is considered an endogenous angiogenic inhibitor. In addition, multiple studies demonstrated that kallistatin directly inhibits cancer cell growth. However, the molecular mechanisms underlying these effects remain unclear. Methods Pull-down, immunoprecipitation, and immunoblotting were used for binding experiments. To elucidate the mechanisms, integrin β3 knockdown (siRNA) or blockage (antibody treatment) on the cell surface of small the cell lung cancer NCI-H446 cell line was used. Results Interestingly, kallistatin was capable of binding integrin β3 on the cell surface of NCI-H446 cells. Meanwhile, integrin β3 knockdown or blockage resulted in loss of antitumor activities induced by kallistatin. Furthermore, kallistatin suppressed tyrosine phosphorylation of integrin β3 and its downstream signaling pathways, including FAK/-Src, AKT and Erk/MAPK. Viability, proliferation and migration of NCI-H446 cells were inhibited by kallistatin, with Bcl-2 and Grb2 downregulation, and Bax, cleaved caspase-9 and caspase 3 upregulation. Conclusions These findings reveal a novel role for kallistatin in preventing small cell lung cancer growth and mobility, by direct interaction with integrin β3, leading to blockade of the related signaling pathway. Focal Adhesion Kinase (dpeaa)DE-He213 Small Cell Lung Cancer Cell (dpeaa)DE-He213 Focal Adhesion Kinase Inhibitor (dpeaa)DE-He213 Pastoris Strain GS115 (dpeaa)DE-He213 Lung Cancer Cell Proliferation (dpeaa)DE-He213 Wang, Xiao aut Huang, Xiaoping aut Yang, Huiyong aut Pang, Suqiu aut Xie, Xiaolan aut Zeng, Shulan aut Lin, Junsheng aut Diao, Yong aut Enthalten in Cancer cell international London : BioMed Central, 2001 16(2016), 1 vom: 01. Dez. (DE-627)355989204 (DE-600)2091573-1 1475-2867 nnns volume:16 year:2016 number:1 day:01 month:12 https://dx.doi.org/10.1186/s12935-016-0365-7 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 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_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 16 2016 1 01 12
language	English
source	Enthalten in Cancer cell international 16(2016), 1 vom: 01. Dez. volume:16 year:2016 number:1 day:01 month:12
sourceStr	Enthalten in Cancer cell international 16(2016), 1 vom: 01. Dez. volume:16 year:2016 number:1 day:01 month:12
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topic_facet	Focal Adhesion Kinase Small Cell Lung Cancer Cell Focal Adhesion Kinase Inhibitor Pastoris Strain GS115 Lung Cancer Cell Proliferation
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container_title	Cancer cell international
authorswithroles_txt_mv	Wang, Guoquan @@aut@@ Wang, Xiao @@aut@@ Huang, Xiaoping @@aut@@ Yang, Huiyong @@aut@@ Pang, Suqiu @@aut@@ Xie, Xiaolan @@aut@@ Zeng, Shulan @@aut@@ Lin, Junsheng @@aut@@ Diao, Yong @@aut@@
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Viability, proliferation and migration of NCI-H446 cells were inhibited by kallistatin, with Bcl-2 and Grb2 downregulation, and Bax, cleaved caspase-9 and caspase 3 upregulation. 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author	Wang, Guoquan
spellingShingle	Wang, Guoquan misc Focal Adhesion Kinase misc Small Cell Lung Cancer Cell misc Focal Adhesion Kinase Inhibitor misc Pastoris Strain GS115 misc Lung Cancer Cell Proliferation Inhibition of integrin β3, a binding partner of kallistatin, leads to reduced viability, invasion and proliferation in NCI-H446 cells
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topic_title	Inhibition of integrin β3, a binding partner of kallistatin, leads to reduced viability, invasion and proliferation in NCI-H446 cells Focal Adhesion Kinase (dpeaa)DE-He213 Small Cell Lung Cancer Cell (dpeaa)DE-He213 Focal Adhesion Kinase Inhibitor (dpeaa)DE-He213 Pastoris Strain GS115 (dpeaa)DE-He213 Lung Cancer Cell Proliferation (dpeaa)DE-He213
topic	misc Focal Adhesion Kinase misc Small Cell Lung Cancer Cell misc Focal Adhesion Kinase Inhibitor misc Pastoris Strain GS115 misc Lung Cancer Cell Proliferation
topic_unstemmed	misc Focal Adhesion Kinase misc Small Cell Lung Cancer Cell misc Focal Adhesion Kinase Inhibitor misc Pastoris Strain GS115 misc Lung Cancer Cell Proliferation
topic_browse	misc Focal Adhesion Kinase misc Small Cell Lung Cancer Cell misc Focal Adhesion Kinase Inhibitor misc Pastoris Strain GS115 misc Lung Cancer Cell Proliferation
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title	Inhibition of integrin β3, a binding partner of kallistatin, leads to reduced viability, invasion and proliferation in NCI-H446 cells
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title_full	Inhibition of integrin β3, a binding partner of kallistatin, leads to reduced viability, invasion and proliferation in NCI-H446 cells
author_sort	Wang, Guoquan
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author_browse	Wang, Guoquan Wang, Xiao Huang, Xiaoping Yang, Huiyong Pang, Suqiu Xie, Xiaolan Zeng, Shulan Lin, Junsheng Diao, Yong
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doi_str_mv	10.1186/s12935-016-0365-7
title_sort	inhibition of integrin β3, a binding partner of kallistatin, leads to reduced viability, invasion and proliferation in nci-h446 cells
title_auth	Inhibition of integrin β3, a binding partner of kallistatin, leads to reduced viability, invasion and proliferation in NCI-H446 cells
abstract	Background Kallistatin is a serine proteinase inhibitor and heparin-binding protein. It is considered an endogenous angiogenic inhibitor. In addition, multiple studies demonstrated that kallistatin directly inhibits cancer cell growth. However, the molecular mechanisms underlying these effects remain unclear. Methods Pull-down, immunoprecipitation, and immunoblotting were used for binding experiments. To elucidate the mechanisms, integrin β3 knockdown (siRNA) or blockage (antibody treatment) on the cell surface of small the cell lung cancer NCI-H446 cell line was used. Results Interestingly, kallistatin was capable of binding integrin β3 on the cell surface of NCI-H446 cells. Meanwhile, integrin β3 knockdown or blockage resulted in loss of antitumor activities induced by kallistatin. Furthermore, kallistatin suppressed tyrosine phosphorylation of integrin β3 and its downstream signaling pathways, including FAK/-Src, AKT and Erk/MAPK. Viability, proliferation and migration of NCI-H446 cells were inhibited by kallistatin, with Bcl-2 and Grb2 downregulation, and Bax, cleaved caspase-9 and caspase 3 upregulation. Conclusions These findings reveal a novel role for kallistatin in preventing small cell lung cancer growth and mobility, by direct interaction with integrin β3, leading to blockade of the related signaling pathway. © The Author(s) 2016
abstractGer	Background Kallistatin is a serine proteinase inhibitor and heparin-binding protein. It is considered an endogenous angiogenic inhibitor. In addition, multiple studies demonstrated that kallistatin directly inhibits cancer cell growth. However, the molecular mechanisms underlying these effects remain unclear. Methods Pull-down, immunoprecipitation, and immunoblotting were used for binding experiments. To elucidate the mechanisms, integrin β3 knockdown (siRNA) or blockage (antibody treatment) on the cell surface of small the cell lung cancer NCI-H446 cell line was used. Results Interestingly, kallistatin was capable of binding integrin β3 on the cell surface of NCI-H446 cells. Meanwhile, integrin β3 knockdown or blockage resulted in loss of antitumor activities induced by kallistatin. Furthermore, kallistatin suppressed tyrosine phosphorylation of integrin β3 and its downstream signaling pathways, including FAK/-Src, AKT and Erk/MAPK. Viability, proliferation and migration of NCI-H446 cells were inhibited by kallistatin, with Bcl-2 and Grb2 downregulation, and Bax, cleaved caspase-9 and caspase 3 upregulation. Conclusions These findings reveal a novel role for kallistatin in preventing small cell lung cancer growth and mobility, by direct interaction with integrin β3, leading to blockade of the related signaling pathway. © The Author(s) 2016
abstract_unstemmed	Background Kallistatin is a serine proteinase inhibitor and heparin-binding protein. It is considered an endogenous angiogenic inhibitor. In addition, multiple studies demonstrated that kallistatin directly inhibits cancer cell growth. However, the molecular mechanisms underlying these effects remain unclear. Methods Pull-down, immunoprecipitation, and immunoblotting were used for binding experiments. To elucidate the mechanisms, integrin β3 knockdown (siRNA) or blockage (antibody treatment) on the cell surface of small the cell lung cancer NCI-H446 cell line was used. Results Interestingly, kallistatin was capable of binding integrin β3 on the cell surface of NCI-H446 cells. Meanwhile, integrin β3 knockdown or blockage resulted in loss of antitumor activities induced by kallistatin. Furthermore, kallistatin suppressed tyrosine phosphorylation of integrin β3 and its downstream signaling pathways, including FAK/-Src, AKT and Erk/MAPK. Viability, proliferation and migration of NCI-H446 cells were inhibited by kallistatin, with Bcl-2 and Grb2 downregulation, and Bax, cleaved caspase-9 and caspase 3 upregulation. Conclusions These findings reveal a novel role for kallistatin in preventing small cell lung cancer growth and mobility, by direct interaction with integrin β3, leading to blockade of the related signaling pathway. © The Author(s) 2016
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title_short	Inhibition of integrin β3, a binding partner of kallistatin, leads to reduced viability, invasion and proliferation in NCI-H446 cells
url	https://dx.doi.org/10.1186/s12935-016-0365-7
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author2	Wang, Xiao Huang, Xiaoping Yang, Huiyong Pang, Suqiu Xie, Xiaolan Zeng, Shulan Lin, Junsheng Diao, Yong
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up_date	2024-07-03T20:24:02.111Z
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It is considered an endogenous angiogenic inhibitor. In addition, multiple studies demonstrated that kallistatin directly inhibits cancer cell growth. However, the molecular mechanisms underlying these effects remain unclear. Methods Pull-down, immunoprecipitation, and immunoblotting were used for binding experiments. To elucidate the mechanisms, integrin β3 knockdown (siRNA) or blockage (antibody treatment) on the cell surface of small the cell lung cancer NCI-H446 cell line was used. Results Interestingly, kallistatin was capable of binding integrin β3 on the cell surface of NCI-H446 cells. Meanwhile, integrin β3 knockdown or blockage resulted in loss of antitumor activities induced by kallistatin. Furthermore, kallistatin suppressed tyrosine phosphorylation of integrin β3 and its downstream signaling pathways, including FAK/-Src, AKT and Erk/MAPK. Viability, proliferation and migration of NCI-H446 cells were inhibited by kallistatin, with Bcl-2 and Grb2 downregulation, and Bax, cleaved caspase-9 and caspase 3 upregulation. 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Inhibition of integrin β3, a binding partner of kallistatin, leads to reduced viability, invasion and proliferation in NCI-H446 cells

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