TMPYP4 exerted antitumor effects in human cervical cancer cells through activation of p38 mitogen-activated protein kinase

Abstract Background The aim of the present study was to investigate the potential effects of the 5,10,15,20‑tetrakis (1‑meth‑ ylpyridinium‑4‑yl) porphyrin (TMPyP4) on the proliferation and apoptosis of human cervical cancer cells and the underlying...

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Autores principales:	Cheng,Ming‑Jun, Cao,Yun‑Gui
Lenguaje:	English
Publicado:	Sociedad de Biología de Chile 2017
Materias:	TMPyP4 p38 MAPK Human cervical cancer cells Proliferation Apoptosis
Acceso en línea:	http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602017000100217
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spelling	oai:scielo:S0716-976020170001002172017-09-15TMPYP4 exerted antitumor effects in human cervical cancer cells through activation of p38 mitogen-activated protein kinaseCheng,Ming‑JunCao,Yun‑Gui TMPyP4 p38 MAPK Human cervical cancer cells Proliferation Apoptosis Abstract Background The aim of the present study was to investigate the potential effects of the 5,10,15,20‑tetrakis (1‑meth‑ ylpyridinium‑4‑yl) porphyrin (TMPyP4) on the proliferation and apoptosis of human cervical cancer cells and the underlying mechanisms by which TMPyP4 exerted its actions. Results After human cervical cancer cells were treated with different doses of TMPyP4, cell viability was determined by 3‑(4,5‑dimethyl‑2‑thiazolyl)‑2,5‑diphenyl‑2‑H‑tetrazolium bromide (MTT) method, the apoptosis was observed by flow cytometry (FCM), and the expression of p38 mitogen‑activated protein kinase (MAPK), phosphated p38 MAPK (p‑p38 MAPK), capase‑3, MAPKAPK2 (MK‑2) and poly ADP‑ribose polymerase (PARP) was measured by Western blot analysis. The analysis revealed that TMPyP4 potently suppressed cell viability and induced the apoptosis of human cervical cancer cells in a dose‑dependent manner. In addition, the up‑regulation of p‑p38 MAPK expression levels was detected in TMPyP4‑treated human cervical cancer cells. However, followed by the block of p38 MAPK signaling pathway using the inhibitor SB203580, the effects of TMPyP4 on proliferation and apoptosis of human cervical cancer cells were significantly changed. Conclusions It was indicated that TMPyP4‑inhibited proliferation and ‑induced apoptosis in human cervical cancer cells was accompanied by activating the p38 MAPK signaling pathway. Taken together, our study demonstrates that TMPyP4 may represent a potential therapeutic method for the treatment of cervical carcinoma.info:eu-repo/semantics/openAccessSociedad de Biología de ChileBiological Research v.50 20172017-01-01text/htmlhttp://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602017000100217en10.1186/s40659-017-0129-4
institution	Scielo Chile
collection	Scielo Chile
language	English
topic	TMPyP4 p38 MAPK Human cervical cancer cells Proliferation Apoptosis
spellingShingle	TMPyP4 p38 MAPK Human cervical cancer cells Proliferation Apoptosis Cheng,Ming‑Jun Cao,Yun‑Gui TMPYP4 exerted antitumor effects in human cervical cancer cells through activation of p38 mitogen-activated protein kinase
description	Abstract Background The aim of the present study was to investigate the potential effects of the 5,10,15,20‑tetrakis (1‑meth‑ ylpyridinium‑4‑yl) porphyrin (TMPyP4) on the proliferation and apoptosis of human cervical cancer cells and the underlying mechanisms by which TMPyP4 exerted its actions. Results After human cervical cancer cells were treated with different doses of TMPyP4, cell viability was determined by 3‑(4,5‑dimethyl‑2‑thiazolyl)‑2,5‑diphenyl‑2‑H‑tetrazolium bromide (MTT) method, the apoptosis was observed by flow cytometry (FCM), and the expression of p38 mitogen‑activated protein kinase (MAPK), phosphated p38 MAPK (p‑p38 MAPK), capase‑3, MAPKAPK2 (MK‑2) and poly ADP‑ribose polymerase (PARP) was measured by Western blot analysis. The analysis revealed that TMPyP4 potently suppressed cell viability and induced the apoptosis of human cervical cancer cells in a dose‑dependent manner. In addition, the up‑regulation of p‑p38 MAPK expression levels was detected in TMPyP4‑treated human cervical cancer cells. However, followed by the block of p38 MAPK signaling pathway using the inhibitor SB203580, the effects of TMPyP4 on proliferation and apoptosis of human cervical cancer cells were significantly changed. Conclusions It was indicated that TMPyP4‑inhibited proliferation and ‑induced apoptosis in human cervical cancer cells was accompanied by activating the p38 MAPK signaling pathway. Taken together, our study demonstrates that TMPyP4 may represent a potential therapeutic method for the treatment of cervical carcinoma.
author	Cheng,Ming‑Jun Cao,Yun‑Gui
author_facet	Cheng,Ming‑Jun Cao,Yun‑Gui
author_sort	Cheng,Ming‑Jun
title	TMPYP4 exerted antitumor effects in human cervical cancer cells through activation of p38 mitogen-activated protein kinase
title_short	TMPYP4 exerted antitumor effects in human cervical cancer cells through activation of p38 mitogen-activated protein kinase
title_full	TMPYP4 exerted antitumor effects in human cervical cancer cells through activation of p38 mitogen-activated protein kinase
title_fullStr	TMPYP4 exerted antitumor effects in human cervical cancer cells through activation of p38 mitogen-activated protein kinase
title_full_unstemmed	TMPYP4 exerted antitumor effects in human cervical cancer cells through activation of p38 mitogen-activated protein kinase
title_sort	tmpyp4 exerted antitumor effects in human cervical cancer cells through activation of p38 mitogen-activated protein kinase
publisher	Sociedad de Biología de Chile
publishDate	2017
url	http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602017000100217
work_keys_str_mv	AT chengming8209jun tmpyp4exertedantitumoreffectsinhumancervicalcancercellsthroughactivationofp38mitogenactivatedproteinkinase AT caoyun8209gui tmpyp4exertedantitumoreffectsinhumancervicalcancercellsthroughactivationofp38mitogenactivatedproteinkinase
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TMPYP4 exerted antitumor effects in human cervical cancer cells through activation of p38 mitogen-activated protein kinase

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