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Updated: Jul 12, 2025

Modeling Oral-Esophageal Squamous Cell Carcinoma in 3D Organoids
Published on: December 23, 2022
ENAH-202 promotes cancer progression in oral squamous cell carcinoma by regulating ZNF502/VIM axis
Xinyue Zhang1,2, Xi Chen1,2, Dongyuan Sun1,2
1School of Stomatology, Weifang Medical University, Weifang, Shandong, China.
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.
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