CMTMS-v1 induces apoptosis in cervical carcinoma cells
CMTMS-v1 induces apoptosis in cervical carcinoma cells
复制标题
CMTM5-v1 诱导宫颈癌细胞凋亡。
DOI：
10.1016/j.bbrc.2008.12.126
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发表时间：
2009-02-20
影响因子：
3.1
通讯作者：
Han, Wenling
中科院分区：
文献类型：
--
作者：
Shao, Luning;Guo, Xiaohuan;Han, Wenling
CMTM 5（含CKLF样MARVEL跨膜结构域的成员5）在包括宫颈癌（CC）细胞在内的各种肿瘤细胞系中表现出肿瘤抑制活性，并伴有频繁的表观遗传失活。在本文中，我们研究了CMTM 5-v1（主要的RNA剪接形式）在HeLa和SiHa细胞中的功能。CMTM 5-v1在两种细胞中的过表达均能诱导细胞凋亡，但在SiHa中的作用比在HeLa中更明显。在SiHa细胞中，CMTM 5-v1的恢复引起线粒体跨膜电位的破坏、细胞色素c的释放、半胱天冬酶3的激活和PARP的裂解。一般的caspase抑制剂几乎阻止SiHa细胞的凋亡，表明CMTM 5-v1主要通过caspase依赖的途径诱导细胞凋亡。这些发现证实CMTM 5-v1通过诱导凋亡抑制CC细胞系的生长。(C)2008年爱思唯尔公司版权所有
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