EMC6/TMEM93 suppresses glioblastoma proliferation by modulating autophagy.
EMC6/TMEM93 suppresses glioblastoma proliferation by modulating autophagy.
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EMC6/TMEM93 通过调节自噬抑制胶质母细胞瘤增殖
DOI：
10.1038/cddis.2015.408
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发表时间：
2016-01-14
影响因子：
9
通讯作者：
Bai Y
中科院分区：
文献类型：
--
作者：
Shen X;Kan S;Hu J;Li M;Lu G;Zhang M;Zhang S;Hou Y;Chen Y;Bai Y
EMC 6（endoplasmic reticulum membrane protein complex subunit 6），又称跨膜蛋白93，是一种新型的自噬正调控因子。在这份报告中，我们评估了EMC 6在体外和体内胶质母细胞瘤细胞中的抗肿瘤活性。我们的数据表明，EMC 6在三个胶质母细胞瘤细胞系（SHG 44，U87和U251）中的过表达通过激活自噬抑制肿瘤细胞生长，但不能诱导细胞凋亡。EMC 6介导的自噬与PIK 3CA/AKT/mTOR信号通路的失活相关。因此，胶质母细胞瘤细胞中的EMC 6敲低具有相反的效果;它促进细胞生长。EMC 6的过表达还使胶质母细胞瘤细胞对化疗药物替莫唑胺敏感，以进一步抑制肿瘤生长。我们的数据表明，EMC 6诱导的自噬可能在抑制胶质母细胞瘤的发展中发挥积极作用。
EMC6 (endoplasmic reticulum membrane protein complex subunit 6), also known as transmembrane protein 93, is a novel positive autophagy regulator. In this report, we evaluated the anti-tumor activity of EMC6 in glioblastoma cells in vitro and in vivo. Our data show that overexpression of EMC6 in three glioblastoma cell lines (SHG44, U87 and U251) suppresses tumor cell growth by activating autophagy, but fails to induce cell apoptosis. EMC6-mediated autophagy was associated with inactivation of the PIK3CA/AKT/mTOR signaling pathway. Accordingly, EMC6 knockdown in glioblastoma cells had the opposite effect; it promoted cell growth. Overexpression of EMC6 also sensitized glioblastoma cells to the chemotherapy drug, temozolomide, to further suppress tumor growth. Our data indicate that EMC6-induced autophagy may play a positive role in suppressing the development of glioblastoma.