Loss of TIM50 suppresses proliferation and induces apoptosis in breast cancer
Loss of TIM50 suppresses proliferation and induces apoptosis in breast cancer
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TIM50 缺失会抑制乳腺癌的增殖并诱导细胞凋亡
DOI：
10.1007/s13277-015-3878-0
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发表时间：
2016-01-01
期刊：
影响因子：
--
通讯作者：
Jin, Wei
中科院分区：
文献类型：
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作者：
Gao, Shui-Ping;Sun, He-Fen;Jin, Wei
TIM50是TIM23复合物的重要组成部分，参与蛋白质转运进入线粒体内膜。在这里，我们发现SILAC增加了乳腺癌细胞中的TIM50。然而，其在乳腺癌中的生物学功能和分子机制知之甚少。为了深入了解TIM50在乳腺癌中的功能，我们构建了两个稳定转染的细胞系，并检测了组织样品中TIM50的表达。我们的数据显示，TIM50在乳腺癌中的表达增加。通过慢病毒介导的shRNA稳定抑制TIM50的表达，显示出抑制癌细胞增殖和诱导凋亡的能力。此外，TIM50的缺失可降低线粒体膜电位，这可能与细胞活力有关。总之，我们的研究结果揭示了TIM50通过降低乳腺癌细胞线粒体膜电位来调节细胞增殖和凋亡的新作用，并表明TIM50可能是控制乳腺癌进展的潜在靶点。
TIM50 is an essential component of TIM23 complex and involved in protein translocating into the inner mitochondrial membrane. Here, we found that TIM50 was increased in breast cancer cells by SILAC. However, its biological functions and molecular mechanisms in breast cancer are poorly understood. To gain insight into the functions of TIM50 in breast cancer, we constructed two stably transfected cell lines and examined TIM50 expression in tissue samples. Our data showed that TIM50 expression was increased in breast cancer. The stable suppression of TIM50 expression through lentivirus-mediated shRNA was shown to inhibit the abilities of cancer cell proliferation and induce apoptosis. What is more, depletion of TIM50 could decrease mitochondrial membrane potential, which may be associated with cell viability. Taken together, our findings reveal a new role for TIM50 in regulating cell proliferation and apoptosis through decreasing mitochondrial membrane potential in breast cancer cell and suggest that TIM50 might be a potential target for controlling breast cancer progression.