CD38 enhances the proliferation and inhibits the apoptosis of cervical cancer cells by affecting the mitochondria functions
CD38 enhances the proliferation and inhibits the apoptosis of cervical cancer cells by affecting the mitochondria functions
复制标题
CD38通过影响线粒体功能促进宫颈癌细胞增殖并抑制凋亡
DOI：
10.1002/mc.22677
复制
发表时间：
2017-10-01
影响因子：
4.6
通讯作者：
Zhou, Yanhong
中科院分区：
文献类型：
--
作者：
Liao, Shan;Xiao, Songshu;Zhou, Yanhong
Cervical cancer is one of the most common malignant tumors in women all over the world. The exact mechanism of occurrence and development of cervical cancer has not been fully elucidated. CD38 is a type II transmembrane glycoprotein, which was found to mediate diverse activities, including signal transduction, cell adhesion, and cyclic ADP‐ribose synthesis. Here, we reported that CD38 promoted cell proliferation and inhibited cell apoptosis in cervical cancer cells by affecting the mitochondria functions. We established stable cervical cancer cell lines with CD38 over‐expressed. CCK8 assay and colony formation assay indicated that CD38 promoted cervical cancer cell proliferation. Nude mouse tumorigenicity assay showed that CD38 significantly promotes tumor growth in vivo. CD38 also induced S phase accumulation in cell cycle analysis and suppressed cell apoptosis in cervical cancer cells. Meanwhile, flow cytometry analysis of mitochondria functions suggested that CD38 decreased intracellular Ca2+ levels in cervical cancer cells and CD38 was involved in down‐regulation of ROS levels and prevented mitochondrial apoptosis in cervical cancer cells. The percentage of cells with loss of mitochondrial membrane potential (Δψm) in CD38‐overexpressed cervical cancer cells was less than control groups. Furthermore, we found an up‐regulation of MDM2, cyclinA1, CDK4, cyclinD1, NF‐kB P65, c‐rel, and a downregulation of P53, P21, and P38 by Western blot analysis. These results indicated that CD38 enhanced the proliferation and inhibited the apoptosis of cervical cancer cells by affecting the mitochondria functions.
