Cancer cell growth is characterized by reprogrammed glucose metabolism and subsequent high rate of glycolysis. The metabolic reprogramming is essential for cell proliferation and drug resistance of cancer cells including glioblastoma (GBM). MicroRNAs play pivotal roles during GBM development. In the present study, we discovered a significant downregulation of miR-1297 in GBM. Decreased miR-1297 expression was associated with prolonged overall survival of patients with glioma. Overexpression of miR-1297 promoted cell proliferation and glycolysis in GBM cells. Bioinformatic analysis (TargetScan and miRanda) indicated that miR-1297 might target 3′UTR of KPNA2, a key regulator of glycolysis in GBM. The regulation was confirmed in a dual-luciferase reporter assay in GBM cells. Furthermore, overexpression of KPNA2 could reverse miR-1297 mimic induced cell growth arrest and inhibition of glycolysis in GBM cells. Finally, a negative correlation between miR-1297 and KPNA2 mRNA levels was observed in GBM tissues. Collectively, the data demonstrated that the abnormal metabolic reprogramming was driven by miR-1297 in GBM and suggested miR-1297 as a tumor suppressor.

中文翻译：

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MiR-1297 通过抑制 KPNA2 负调控胶质母细胞瘤的代谢重编程。

癌细胞生长的特征在于重新编程的葡萄糖代谢和随后的高糖酵解速率。代谢重编程对于包括胶质母细胞瘤 (GBM) 在内的癌细胞的细胞增殖和耐药性至关重要。MicroRNAs 在 GBM 发育过程中发挥着关键作用。在本研究中，我们发现 GBM 中 miR-1297 显着下调。降低的 miR-1297 表达与延长胶质瘤患者的总生存期有关。miR-1297的过表达促进GBM细胞中的细胞增殖和糖酵解。生物信息学分析（TargetScan 和 miRanda）表明 miR-1297 可能靶向 KPNA2 的 3'UTR，KPNA2 是 GBM 中糖酵解的关键调节剂。在 GBM 细胞中的双荧光素酶报告基因测定中证实了该调节。此外，KPNA2 的过表达可以逆转 miR-1297 模拟诱导的细胞生长停滞和 GBM 细胞中糖酵解的抑制。最后，在 GBM 组织中观察到 miR-1297 和 KPNA2 mRNA 水平呈负相关。总的来说，数据表明异常代谢重编程是由 GBM 中的 miR-1297 驱动的，并表明 miR-1297 是一种肿瘤抑制因子。