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Title 

Mitomycin C induces apoptosis via Fas/FasL dependent pathway and suppression of IL-18 in cervical carcinoma cells

Authors 

Yun Hee KangKyung Ae LeeChun Jeih RyuHee Gu LeeJ S LimS N ParkS G PaikDo Young Yoon

Publisher 

Elsevier

Issue Date 

2006

Citation 

Cancer Letters, vol. 237, no. 1, pp. 33-44

Keywords 

apoptosiscaspase-8cervical carcinoma cellsFasLinterleukin-18mitomycin Ccarboplatincaspase 3caspase 8cisplatin

Abstract 

Mitomycin C (MMC) is used fairly widely as an anticancer drug, as it possesses mechanisms of action which are preferable to other chemotherapeutic compounds, including cisplatin, docetaxel, and lovastatin. In the previous study, we established the RSV-luc promoter analysis system, which is used to screen drugs against cervical carcinomas caused by HPV infection. We then demonstrated the repression of HPV E6-activated RSV promoter activity by anticancer agents such as carboplatin (CA), cisplatin (CIS), and MMC. In these studies, we focused on the investigation of apoptotic mechanisms in MMC-treated cervical carcinoma cell lines, most notably SiHa/pRSV-luc (KCTC 0427BP) and SiHa. DNA fragmentation assays and TUNEL staining revealed that MMC and CIS, but not CA, resulted in apoptosis. MMC treatment induced a reduction in the expressions of the E6 oncogene and IL-18, in a p53-independent manner. MMC also increased FasL expression and induced the processing of caspases-8 and -3. Our results indicated that MMC induced apoptosis in SiHa/pRSV-luc and SiHa cells via caspase-8 and -3 processing, in a Fas/FasL-dependent manner. MMC also suppressed the expression of IL-18 in the same cells. MMC also down-regulated IκB expression, and up-regulated p65 expression. These results suggest that MMC induces apoptosis, not only through caspase-8 and -3 dependent Fas/FasL pathway, but also via the regulation of NF-κB activity and IL-18 expression.

ISSN 

0304-3835

Link 

http://dx.doi.org/10.1016/j.canlet.2005.05.043

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2017-04-19


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