Abstract
BackgroundThe 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.ResultsAfter 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.ConclusionsIt 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.
Highlights
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
TMPyP4 inhibited the proliferation rates of human cervical cancer cells To investigate the roles of TMPyP4 in human cervical cancer cells, we performed the MTT assay to evaluate the changes of cell viability
These results indicated that TMPyP4 had low cytotoxic effects on human normal cells and inhibited cell proliferation in human cervical cancer cells
Summary
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. Human papillomavirus (HPV) types is recognized as an essential precursor to the development of cervical cancer. It has been reported that TMPyP4 leads to the arrest of tumor cell growth, and induces the apoptosis of tumor cells through reducing the telomerase activity [7,8,9], indicating that TMPyP4 presents a potential therapeutic target in tumor cells. It is crucial to comprehensively understand biological effects of TMPyP4 in tumor cells before it can be used for anti-cancer therapeutics. We evaluated the effects of TMPyP4 on the proliferation and apoptosis of human cervical cancer cells and further explored its underlying mechanisms
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