我们旨在论证长链非编码RNA（lncRNA）ENAH-202对口腔鳞状细胞癌（OSCC）发生发展的调控作用及其分子机制。我们通过定量实时检测ENAH-202在OSCC组织和细胞系中的表达。实时PCR（qPCR）。使用 CCK-8、集落形成测定、Transwell 测定、异种移植物形成和尾静脉注射在体外和体内评估 ENAH-202 的生物学功能。通过 RNA Pull-down、LS-MS/MS 分析、RNA 免疫沉淀 (RIP) 和染色质免疫沉淀 (ChIP) 测定，确定了 ENAH-202 促进 OSCC 进展的进一步分子机制。ENAH-202 在 OSCC 组织中显着上调和细胞。 ENAH-202 在体外和体内促进 OSCC 细胞增殖、迁移和侵袭。启用同系物（ENAH）和上皮间质转化（EMT）相关蛋白的表达随着ENAH-202的表达而变化。此外，ENAH-202通过与ZNF502结合促进波形蛋白（VIM）的转录，这可以帮助ENAH-202促进OSCC进展。ENAH-202通过调节ZNF502/VIM轴促进OSCC细胞增殖和转移，在OSCC细胞增殖和转移中发挥重要作用。 OSCC 进展。© 2023 作者。约翰·威利出版的癌症医学

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 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.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.ENAH-202 facilitated OSCC cell proliferation and metastasis by regulating ZNF502/VIM axis, which played an important role in OSCC progression.© 2023 The Authors. Cancer Medicine published by John Wiley & Sons Ltd.