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<p>Cervical squamous cell carcinoma (CSCC), the most prevalent form of cervical cancer, is often diagnosed at advanced stages with limited treatment efficacy. Cell migration and invasion are critical steps, yet its molecular mechanisms remain poorly understood. This study investigates the role of the long non‑coding RNA DLEU2 in CSCC migration and invasion. RNA sequencing of 7 invasive CSCC and 7 normal cervical tissues revealed significant upregulation of DLEU2 in tumors, which correlated with poor prognosis in advanced‑stage patients. Functionally, DLEU2 knockdown suppressed, while its overexpression promoted, cancer cell migration and invasion in vitro. Mechanistically, we identified a DLEU2/E2F1 regulatory axis: E2F1 transcriptionally activates DLEU2, and DLEU2 in turn interacts with and may regulate E2F1 at transcription and post‑transcriptional level. Ectopic overexpression of E2F1 rescued the migratory and invasive impairments induced by DLEU2 silencing. Furthermore, DLEU2 regulated key migration and invasion‑related genes, including SNAI2 and MMP9. Together, our findings suggest an association between DLEU2 and E2F1 that may contribute to pro-migratory and pro-invasive phenotypes in CSCC, potentially offering this axis as a candidate therapeutic target.</p>

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A DLEU2/E2F1 regulatory axis promotes migration and invasion phenotypes in cervical squamous cell carcinoma

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月6日

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  • Min He,
  • Shiyi Huang,
  • Mingjiang Wang,
  • Tangrui Zhu,
  • Jinhua Ding,
  • Yitao Wang,
  • Mingbo Liu,
  • Hanlu Wen

摘要

Cervical squamous cell carcinoma (CSCC), the most prevalent form of cervical cancer, is often diagnosed at advanced stages with limited treatment efficacy. Cell migration and invasion are critical steps, yet its molecular mechanisms remain poorly understood. This study investigates the role of the long non‑coding RNA DLEU2 in CSCC migration and invasion. RNA sequencing of 7 invasive CSCC and 7 normal cervical tissues revealed significant upregulation of DLEU2 in tumors, which correlated with poor prognosis in advanced‑stage patients. Functionally, DLEU2 knockdown suppressed, while its overexpression promoted, cancer cell migration and invasion in vitro. Mechanistically, we identified a DLEU2/E2F1 regulatory axis: E2F1 transcriptionally activates DLEU2, and DLEU2 in turn interacts with and may regulate E2F1 at transcription and post‑transcriptional level. Ectopic overexpression of E2F1 rescued the migratory and invasive impairments induced by DLEU2 silencing. Furthermore, DLEU2 regulated key migration and invasion‑related genes, including SNAI2 and MMP9. Together, our findings suggest an association between DLEU2 and E2F1 that may contribute to pro-migratory and pro-invasive phenotypes in CSCC, potentially offering this axis as a candidate therapeutic target.