Rab-like 3 (RABL3) is a member of Rab family that is related with several kinds of cancers. However, the functional roles of RABL3 in oral squamous cell carcinoma (OSCC) remain largely unknown. In the current study, we examined the expression levels of RABL3 in OSCC tissues and cell lines. The results showed that RABL3 expression was markedly increased in OSCC tissues and cell lines. Knockdown of RABL3 significantly suppressed the proliferation, migration and invasion of OSCC cells. Overexpression of RABL3 exhibited opposite effects with RABL3 knockdown. In vivo assay demonstrated that knockdown of RABL3 suppressed the tumorigenesis of OSCC. Moreover, RABL3 regulated the activation of focal adhesion kinase (FAK)/protein kinase B (Akt) signaling pathway in OSCC cells. Inhibition of FAK reversed the effects of RABL3 overexpression on cell proliferation, migration and invasion of OSCC cells. In conclusion, these findings demonstrated that RABL3 acted as an oncogene in OSCC, which was attributed to the regulation of FAK/Akt pathway. Thus, RABL3 may be potential therapeutic target for the treatment of OSCC.

Rab-like 3 (RABL3) 是与多种癌症相关的 Rab 家族成员。然而，RABL3 在口腔鳞状细胞癌 (OSCC) 中的功能作用仍然很大程度上未知。在目前的研究中，我们检测了 RABL3 在 OSCC 组织和细胞系中的表达水平。结果表明，RABL3在OSCC组织和细胞系中的表达明显增加。敲除RABL3显着抑制OSCC细胞的增殖、迁移和侵袭。RABL3 的过表达表现出与 RABL3 敲低相反的效果。体内测定表明，RABL3的敲低抑制了OSCC的肿瘤发生。此外，RABL3 调节 OSCC 细胞中粘着斑激酶 (FAK)/蛋白激酶 B (Akt) 信号通路的激活。FAK的抑制逆转了RABL3过表达对OSCC细胞增殖、迁移和侵袭的影响。总之，这些发现表明 RABL3 在 OSCC 中充当癌基因，这归因于 FAK/Akt 通路的调节。因此，RABL3 可能是治疗 OSCC 的潜在治疗靶点。