Background: 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.
Methods: 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 in vitro and in vivo 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.
Results: ENAH-202 was significantly upregulated in OSCC tissues and cells. ENAH-202 promoted OSCC cell proliferation, migration, and invasion in vitro and in vivo. 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.
Conclusions: ENAH-202 facilitated OSCC cell proliferation and metastasis by regulating ZNF502/VIM axis, which played an important role in OSCC progression.
Keywords: ENAH-202; ZNF502; cancer progression; epithelial-to-mesenchymal transition; long non-coding RNA; oral squamous cell carcinoma.
© 2023 The Authors. Cancer Medicine published by John Wiley & Sons Ltd.