Knockdown of RABL3 suppresses the proliferation and invasion of oral squamous cell carcinoma through inactivating the FAK/AKT pathway.

Abstract

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.