Abstract：
Gliomas are the most common central nervous system tumours; they are highly aggressive and have a poor prognosis. RGS16 belongs to the regulator of G-protein signalling (RGS) protein family, which plays an important role in promoting various cancers, such as breast cancer, pancreatic cancer, and colorectal cancer. Moreover, previous studies confirmed that let-7c-5p, a well-known microRNA, can act as a tumour suppressor to regulate the progression of various tumours by inhibiting the expression of its target genes. However, whether RGS16 can promote the progression of glioma and whether it is regulated by miR let-7c-5p are still unknown. Here, we confirmed that RGS16 is upregulated in glioma tissues and that high expression of RGS16 is associated with poor survival. Ectopic deletion of RGS16 significantly suppressed glioma cell proliferation and migration both in vitro and in vivo. Moreover, RGS16 was validated as a direct target gene of miR let-7c-5p. The overexpression of miR let-7c-5p obviously downregulated the expression of RGS16, and knocking down miR let-7c-5p had the opposite effect. Thus, we suggest that the suppression of RGS16 by miR let-7c-5p can promote glioma progression and may serve as a potential prognostic biomarker and therapeutic target in glioma.
摘要：
胶质瘤是最常见的中枢神经系统肿瘤；它们具有高度侵袭性，预后不良。RGS16属于G蛋白信号（RGS）蛋白家族的调节因子，在促进各种癌症中起着重要作用，比如乳腺癌，胰腺癌,还有结直肠癌.此外，之前的研究证实let-7c-5p，一种众所周知的microRNA,可以作为肿瘤抑制因子，通过抑制其靶基因的表达来调节各种肿瘤的进展。然而,RGS16是否能促进胶质瘤的进展以及是否受miRlet-7c-5p调控尚不清楚。这里,我们证实RGS16在神经胶质瘤组织中上调,RGS16的高表达与低生存率相关.RGS16的异位缺失在体外和体内均显着抑制了神经胶质瘤细胞的增殖和迁移。此外，RGS16被验证为miRlet-7c-5p的直接靶基因。miRlet-7c-5p的过表达明显下调RGS16的表达，而敲低miRlet-7c-5p则具有相反的作用。因此，我们提示miRlet-7c-5p抑制RGS16可促进神经胶质瘤的进展,并可作为神经胶质瘤潜在的预后生物标志物和治疗靶点.
