Oral cancer being one of the lethal cancers is generally detected at advanced stages and causes significant mortality world over. The unavailability of the reliable biomarkers and therapeutic targets/agents forms a bottleneck in the treatment of oral cancer. MicroRNAs are considered of immense therapeutic potential for the treatment of cancer. Consistently, in this study the role and therapeutic potential of miR-650 was explored in oral cancer. The analysis of miR-650 expression by qRT-PCR revealed significant (p < 0.05) upregulation of miR-650 in oral cancer cell lines. Cell cycle analysis by flow cytometery revealed that suppression of miR-650 significantly (p < 0.05) inhibits the proliferation of the SCC-25 cells by prompting Sub-G1 cell cycle arrest. Further, miR-650 suppression also inhibited the migration and invasion of the SCC-25 oral cancer cells as revealed by transwell assays. TargetScan analysis showed that miR-650 targets Growth factor independent 1 (Gfi1). Moreover, the results of western blot analysis showed that miR-650 suppression inhibits the expression of Gfi1. Interestingly, suppression of Gfi1 exhibited similar effects on cell proliferation, migration and invasion of the oral cancer cells as that of miR-650 suppression. Nonetheless, miR-650 promoted the proliferation, migration and invasion of the SCC-25 cells by upregulating the expression of Gfi1. Moreover, overexpression of miR-650 could not rescue the effects of Gfi1 silencing on SCC-25 oral cancer cells. Conversely, overexpression of Gfi1 could rescue the effects of miR-650 inhibition on SCC-25 cell proliferation, migration and invasion. Additionally, miR-650 suppression could also inhibit the xenografted tumor growth in vivo by inhibiting the expression of Gfi1. Taken together, miR-650 may prove to be an important therapeutic target for the management of oral cancers.

口腔癌是致命癌症之一，通常在晚期被发现，并在世界范围内导致大量死亡率。可靠的生物标志物和治疗靶点/药物的不可用性形成了口腔癌治疗的瓶颈。MicroRNA 被认为具有治疗癌症的巨大治疗潜力。一致地，在本研究中探索了 miR-650 在口腔癌中的作用和治疗潜力。通过 qRT-PCR 对 miR-650 表达的分析揭示了 口腔癌细胞系中 miR-650 的显着 ( p < 0.05) 上调。通过流式细胞仪进行的细胞周期分析表明，miR-650 的抑制显着 ( p < 0.05) 通过促使 Sub-G1 细胞周期停滞来抑制 SCC-25 细胞的增殖。此外，miR-650 抑制还抑制了 SCC-25 口腔癌细胞的迁移和侵袭，正如 transwell 测定所揭示的那样。TargetScan 分析显示 miR-650 靶向生长因子独立 1 (Gfi1)。此外，western blot 分析的结果表明，抑制 miR-650 会抑制 Gfi1 的表达。有趣的是，抑制 Gfi1 对口腔癌细胞的细胞增殖、迁移和侵袭表现出与抑制 miR-650 相似的作用。尽管如此，miR-650通过上调Gfi1的表达促进了SCC-25细胞的增殖、迁移和侵袭。此外，miR-650 的过表达无法挽救 Gfi1 沉默对 SCC-25 口腔癌细胞的影响。反过来，Gfi1 的过表达可以挽救 miR-650 抑制对 SCC-25 细胞增殖、迁移和侵袭的影响。此外，抑制 miR-650 也可以抑制异种移植肿瘤的生长在体内通过抑制 Gfi1 的表达。总之，miR-650 可能被证明是治疗口腔癌的重要治疗靶点。