MicroRNA-132 cause apoptosis of glioma cells through blockade of the SREBP-1c metabolic pathway related to SIRT1

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• 作者：Yunjun Li^a ; ^b ; ¹ ; Jinqian Zhang^c ; ¹ ; ^{jingwanghou@163.com" class="auth_mail" title="E-mail the corresponding author} ; Jingliang He^d ; Wenjie Zhou^d ; Guoan Xiang^d ; Ruxiang Xu^a ; ^b ; ^{jianshengliylp@163.com" class="auth_mail" title="E-mail the corresponding author}
• 关键词：HMGCR ; 3-hydroxy-3-methylglutaryl CoA reductase ; FASN ; fatty acid synthase ; BDNF ; brain derived neurotrophic factor ; CREB ; cAMP-response element binding protein
• 刊名：Biomedicine & Pharmacotherapy
• 出版年：2016
• 出版时间：March 2016
• 年：2016
• 卷：78
• 期：Complete
• 页码：177-184
• 全文大小：1924 K

文摘

The inhibition role of miRNA (microRNA or miR) on cancer signaling pathways has been used to prospective cancer treatment. SIRT1 might promote tumorigenesis in human glioma.

Methods

Here, we investigated whether miR-132 regulate the expression of SIRT1 and its downstream SREBP (Sterol regulatory element-binding protein)-lipogenesis-cholesterogenesis metabolic pathway in human glioma cells. Furthermore, we studied the effect on biology function of glioma cell induced by miR-132.

Results

MiR-132 inhibited SIRT1 and SREBP-1c expression and downregulated their targeted genes, including HMGCR and FASN. MiR-132 suppressed the cell growth, tumorigenicity, the invasion of glioma cells and migration as well as promoted their apoptosis. The pathways associated with cancer progression and tumorigenicity, and induce glioma cell apoptosis has been inhibited by miR-132 involving in a caspase-dependent apoptotic mechanism.

Conclusions

The recovery of miR-132 resulted in caspase-dependent apoptotic death in glioma cells. MiR-132 that was newly discovered represents a newly targeting mechanism in treatment for glioma.