ENAH-202 promotes cancer progression in oral squamous cell carcinoma by regulating ZNF502/VIM axis.

Abstract

We aimed to demonstrate the regulatory effect of long non-coding RNA (lncRNA) ENAH-202 on oral squamous cell carcinoma (OSCC) development as well as its molecular mechanism. We detected ENAH-202 expression in OSCC tissues and cell lines by quantitative real-time PCR (qPCR). The biological function of ENAH-202 was assessed invitro and invivo using CCK-8, colony formation assays, transwell assays, xenograft formation, and tail vein injection. The further molecular mechanism by which ENAH-202 promoted OSCC progression was identified using RNA pull-down, LS-MS/MS analysis, RNA immunoprecipitation (RIP), and chromatin immunoprecipitation (ChIP) assays. ENAH-202 was significantly upregulated in OSCC tissues and cells. ENAH-202 promoted OSCC cell proliferation, migration, and invasion invitro and invivo. The expression of enabled homolog (ENAH) and epithelial-to-mesenchymal transition (EMT)-related proteins was changed with the expression of ENAH-202. Moreover, ENAH-202 promoted the transcription of Vimentin (VIM) by binding with ZNF502, which can help ENAH-202 promote OSCC progression. ENAH-202 facilitated OSCC cell proliferation and metastasis by regulating ZNF502/VIM axis, which played an important role in OSCC progression.