Department of Neurosurgery, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China.
Neurosci Lett. 2012 Sep 13;525(2):168-72. doi: 10.1016/j.neulet.2012.07.025. Epub 2012 Jul 31.
In mammalian cells, SIRT1 decreases PTEN acetylation and inactivates the AKT pathway in a SIRT1 deacetylase-dependent manner. However, the function of SIRT1 in glioma was unknown. SIRT1 reexpression or knockdown was induced in human glioma cell lines. The cell synchronization, BrdU labeling and mitotic index were detected. Subsequently, cell cycle, cell viability, apoptosis, cell growth and proliferation were analyzed. Our work identified that SIRT1-knockdown significantly delayed mitotic entry of glioma cells, inhibited its growth and proliferation, and promoted its apoptosis. The apoptosis was related to PTEN/PI3K/AKT signaling pathway. The results showed that SIRT1 might be a promoter factor on tumorigenesis of glioma through PTEN/PI3K/AKT signaling pathway.
在哺乳动物细胞中，SIRT1 通过 SIRT1 去乙酰化酶依赖的方式降低 PTEN 的乙酰化并使 AKT 通路失活。然而，SIRT1 在神经胶质瘤中的功能尚不清楚。在人神经胶质瘤细胞系中诱导 SIRT1 重新表达或敲低。检测细胞同步化、BrdU 标记和有丝分裂指数。随后，分析细胞周期、细胞活力、细胞凋亡、细胞生长和增殖。我们的工作表明，SIRT1 敲低显著延迟神经胶质瘤细胞进入有丝分裂，抑制其生长和增殖，并促进其凋亡。凋亡与 PTEN/PI3K/AKT 信号通路有关。结果表明，SIRT1 可能通过 PTEN/PI3K/AKT 信号通路成为神经胶质瘤发生的促进因子。
