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TMPYP4通过激活p38丝裂原活化蛋白激酶在人宫颈癌细胞中发挥抗肿瘤作用。

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

作者信息

Cheng Ming-Jun, Cao Yun-Gui

机构信息

Department of Gynaecology, Shanghai Jiading District Maternal and Child Care Hospital, No. 1216, Gaotai Road, Jiading District, Shanghai, 201821, China.

出版信息

Biol Res. 2017 Jul 3;50(1):24. doi: 10.1186/s40659-017-0129-4.

DOI:10.1186/s40659-017-0129-4
PMID:28673331
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5496143/
Abstract

BACKGROUND

The aim of the present study was to investigate the potential effects of the 5,10,15,20-tetrakis (1-methylpyridinium-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.

摘要

背景

本研究旨在探讨5,10,15,20-四（1-甲基吡啶-4-基）卟啉（TMPyP4）对人宫颈癌细胞增殖和凋亡的潜在影响及其作用的潜在机制。

结果

用不同剂量的TMPyP4处理人宫颈癌细胞后，采用3-（4,5-二甲基-2-噻唑基）-2,5-二苯基-2-H-溴化四唑（MTT）法测定细胞活力，通过流式细胞术（FCM）观察细胞凋亡情况，并用蛋白质免疫印迹法检测p38丝裂原活化蛋白激酶（MAPK）、磷酸化p38 MAPK（p-p38 MAPK）、半胱天冬酶-3、丝裂原活化蛋白激酶相关激酶2（MK-2）和聚ADP-核糖聚合酶（PARP）的表达。分析结果显示，TMPyP4能有效抑制人宫颈癌细胞的活力，并以剂量依赖的方式诱导细胞凋亡。此外，在经TMPyP4处理的人宫颈癌细胞中检测到p-p38 MAPK表达水平上调。然而，在用抑制剂SB203580阻断p38 MAPK信号通路后，TMPyP4对人宫颈癌细胞增殖和凋亡的影响发生了显著变化。

结论

表明TMPyP4抑制人宫颈癌细胞增殖并诱导其凋亡与激活p38 MAPK信号通路有关。综上所述，我们的研究表明TMPyP4可能是一种治疗宫颈癌的潜在治疗方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a059/5496143/ebdd0ba561c2/40659_2017_129_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a059/5496143/8225c344d036/40659_2017_129_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a059/5496143/776d64397ca0/40659_2017_129_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a059/5496143/36cd639a161e/40659_2017_129_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a059/5496143/0b90d5071619/40659_2017_129_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a059/5496143/ebdd0ba561c2/40659_2017_129_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a059/5496143/8225c344d036/40659_2017_129_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a059/5496143/776d64397ca0/40659_2017_129_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a059/5496143/36cd639a161e/40659_2017_129_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a059/5496143/0b90d5071619/40659_2017_129_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a059/5496143/ebdd0ba561c2/40659_2017_129_Fig5_HTML.jpg

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