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Background <p>Aberrant long non-coding RNA (lncRNA) expression regulates tumor progression. With rising incidence, oral squamous cell carcinoma (OSCC) requires mechanistic study. LncRNA functions in OSCC remain unclear.</p> Methods <p>Bioinformatics analysis was conducted to screen the highly expressed lncRNA AC116914.2 associated with m6A methylation in OSCC from The Cancer Genome Atlas database. Techniques including IHC, Western Blot, qPCR, cell functional assays, and in-vivo tumor formation were applied to assess the effects of AC116914.2 on OSCC malignant behaviors and fibroblast functions. Dual-luciferase assays explored the interactions among AC116914.2, miR-1245a, and ZNF250, while ChIP-qPCR verified ZNF250’s regulatory effect on METTL3.</p> Results <p>LncRNA AC116914.2 showed differential expression between tumor and normal tissues. Its knockdown significantly inhibited OSCC progression in vitro and in vivo. Mechanistically, AC116914.2 competitively bound to miR-1245a to maintain ZNF250 levels, stabilizing the oncogene METTL3 expression. Additionally, AC116914.2 promoted extracellular vesicle release and activated cancer-associated fibroblasts, fostering an OSCC-favorable microenvironment.</p> Conclusion <p>This study shows that lncRNA AC116914.2, as a competing endogenous RNA (ceRNA), regulates the expression of METTL3 by competitively binding to miR-1245a with ZNF250, thus promoting OSCC progression. The discovery of this regulatory axis provides new diagnostic markers and therapeutic targets for OSCC.</p>

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LncRNA AC116914.2 promotes the progression of oral cancer by targeting METTL3 via miR-1245a/ZNF250

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月7日

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  • Chunyu Feng,
  • Xinyu Dou,
  • Xiaoshuai Xu,
  • Zihan Dang,
  • Zihan Jiang,
  • Erhui Jiang,
  • Zhengjun Shang

摘要

Background

Aberrant long non-coding RNA (lncRNA) expression regulates tumor progression. With rising incidence, oral squamous cell carcinoma (OSCC) requires mechanistic study. LncRNA functions in OSCC remain unclear.

Methods

Bioinformatics analysis was conducted to screen the highly expressed lncRNA AC116914.2 associated with m6A methylation in OSCC from The Cancer Genome Atlas database. Techniques including IHC, Western Blot, qPCR, cell functional assays, and in-vivo tumor formation were applied to assess the effects of AC116914.2 on OSCC malignant behaviors and fibroblast functions. Dual-luciferase assays explored the interactions among AC116914.2, miR-1245a, and ZNF250, while ChIP-qPCR verified ZNF250’s regulatory effect on METTL3.

Results

LncRNA AC116914.2 showed differential expression between tumor and normal tissues. Its knockdown significantly inhibited OSCC progression in vitro and in vivo. Mechanistically, AC116914.2 competitively bound to miR-1245a to maintain ZNF250 levels, stabilizing the oncogene METTL3 expression. Additionally, AC116914.2 promoted extracellular vesicle release and activated cancer-associated fibroblasts, fostering an OSCC-favorable microenvironment.

Conclusion

This study shows that lncRNA AC116914.2, as a competing endogenous RNA (ceRNA), regulates the expression of METTL3 by competitively binding to miR-1245a with ZNF250, thus promoting OSCC progression. The discovery of this regulatory axis provides new diagnostic markers and therapeutic targets for OSCC.