Department of Cell Biology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, China.
Key Laboratory of Medical Immunology, Ministry of Health, Peking University Health Science Center, Beijing, China.
Cell Death Dis. 2016 Jan 14;7(1):e2043. doi: 10.1038/cddis.2015.408.
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.
EMC6(内质网膜蛋白复合物亚基 6),也称为跨膜蛋白 93,是一种新型的自噬正向调控因子。在本报告中,我们评估了 EMC6 在体外和体内对神经胶质瘤细胞的抗肿瘤活性。我们的数据表明,在三种神经胶质瘤细胞系(SHG44、U87 和 U251)中过表达 EMC6 通过激活自噬来抑制肿瘤细胞生长,但不能诱导细胞凋亡。EMC6 介导的自噬与 PIK3CA/AKT/mTOR 信号通路的失活有关。因此,在神经胶质瘤细胞中敲低 EMC6 会产生相反的效果,促进细胞生长。过表达 EMC6 还能使神经胶质瘤细胞对化疗药物替莫唑胺敏感,进一步抑制肿瘤生长。我们的数据表明,EMC6 诱导的自噬可能在抑制神经胶质瘤的发展中发挥积极作用。