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<p>Cervical cancer (CC) remains a significant global health burden despite advances in prevention and screening. Emerging evidence highlights the critical role of long non-coding RNAs (lncRNAs) and RNA modifications in tumorigenesis. Here, we identified LINC01094 as a highly expressed lncRNA in CC through TCGA analysis and clinical specimens. Functional studies, including CCK-8 method, flow cytometry, Transwell and Western blot assays, demonstrated that LINC01094 knockdown suppressed cell proliferation, migration, and epithelial-mesenchymal transition while promoting apoptosis in CC cells (Caski and SiHa). Mechanistically, NSUN2-mediated 5-methylcytosine methylation stabilized LINC01094, enhancing its expression in CC. Furthermore, LINC01094 facilitated ZNF582-dependent transcriptional activation of SIRT1, promoted the deacetylation and degradation of p53. Rescue experiments confirmed that ectopic expression of either LINC01094 or SIRT1 reversed the tumor-suppressive effects of NSUN2 or LINC01094 knockdown, respectively. Collectively, NSUN2-mediated stabilization of LINC01094 upregulated SIRT1 expression, thereby suppressing the p53 pathway and accelerating CC progression. These findings uncover a novel NSUN2/LINC01094/SIRT1 axis as an epigenetic-transcriptional driver of CC, offering potential therapeutic targets.</p>

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m5c-modified LINC01094 participates in epithelial-mesenchymal transition and metastasis of cervical cancer cells via the ZNF582-SIRT1/p53 axis

  • 期刊论文

  • 发表日期：

    2026年2月3日

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  • Xia Lu,
  • Lili Yao,
  • Xu Xu,
  • Mayinuer Guli Rexiti,
  • Xiaoli He,
  • Yanyan Yang

摘要

Cervical cancer (CC) remains a significant global health burden despite advances in prevention and screening. Emerging evidence highlights the critical role of long non-coding RNAs (lncRNAs) and RNA modifications in tumorigenesis. Here, we identified LINC01094 as a highly expressed lncRNA in CC through TCGA analysis and clinical specimens. Functional studies, including CCK-8 method, flow cytometry, Transwell and Western blot assays, demonstrated that LINC01094 knockdown suppressed cell proliferation, migration, and epithelial-mesenchymal transition while promoting apoptosis in CC cells (Caski and SiHa). Mechanistically, NSUN2-mediated 5-methylcytosine methylation stabilized LINC01094, enhancing its expression in CC. Furthermore, LINC01094 facilitated ZNF582-dependent transcriptional activation of SIRT1, promoted the deacetylation and degradation of p53. Rescue experiments confirmed that ectopic expression of either LINC01094 or SIRT1 reversed the tumor-suppressive effects of NSUN2 or LINC01094 knockdown, respectively. Collectively, NSUN2-mediated stabilization of LINC01094 upregulated SIRT1 expression, thereby suppressing the p53 pathway and accelerating CC progression. These findings uncover a novel NSUN2/LINC01094/SIRT1 axis as an epigenetic-transcriptional driver of CC, offering potential therapeutic targets.