| Title | CMTMS-v1 induces apoptosis in cervical carcinoma cells |
| Authors | Shao, Luning Guo, Xiaohuan Plate, Markus Li, Ting Wang, Yu Ma, Dalong Han, Wenling |
| Affiliation | Peking Univ, Ctr Human Dis Genom, Dept Immunol, Hlth Sci Ctr, Beijing 100191, Peoples R China. Peking Univ, Ctr Human Dis Genom, Dept Immunol, Hlth Sci Ctr, 38 Xueyuan Rd, Beijing 100191, Peoples R China. |
| Keywords | CMTM5 Cervical carcinoma Apoptosis Tumorigenesis CHEMOKINE-LIKE FACTOR-1 FACTOR SUPERFAMILY MOLECULAR-CLONING CYTOCHROME-C PATHWAY TESTIS DEATH FORM |
| Issue Date | 2009 |
| Publisher | 生物化学与生物物理学研究通讯 |
| Citation | BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS.2009,379,(4),866-871. |
| Abstract | CMTM5 (CKLF-like MARVEL transmembrane domain-containing member 5) exhibits tumor inhibition activity with frequent epigenetic inactivation in various tumor cell lines including cervical carcinoma (CC) cells. In this paper, we examined the function of CMTM5-v1 (the primary RNA splicing form) in both HeLa and SiHa cells. Overexpression of CMTM5-v1 in both cells can induce apoptosis, but the effects are more obvious in SiHa than that in HeLa. In SiHa cells, restoration of CMTM5-v1 caused disruption of mitochondrial transmembrane potential, release of cytochrome c, activation of caspase3 and cleavage of PARP. General caspase inhibitor almost prevented apoptosis of SiHa cells, suggesting that CMTM5-v1 induces apoptosis mainly through caspase-dependent pathway. These findings verify that CMTM5-v1 inhibits the growth of CC cell lines via inducing apoptosis. (C) 2008 Elsevier Inc. All rights reserved |
| URI | http://hdl.handle.net/20.500.11897/197313 |
| ISSN | 0006-291X |
| DOI | 10.1016/j.bbrc.2008.12.126 |
| Indexed | SCI(E) PubMed |
| Appears in Collections: | 医学部待认领 |
