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Background <p>Laryngeal cancer is a leading global cause of cancer-related mortality. The regulatory interplay between dysregulated microRNA-761 (miR-761) and oncogenic signaling pathways in laryngeal carcinogenesis has not been fully elucidated‌.</p> Methods <p>This study explored the interaction between miR-761 and programmed cell death protein 4 (PDCD4) through dual-luciferase assay, cell proliferation and migration assays, and xenograft models.</p> Results <p>MiR-761 was significantly upregulated in laryngeal cancer tissues and cell lines, inversely correlating with PDCD4 downregulation. Computational predictions and dual-luciferase assays confirmed that miR-761 targets the 3’-UTR of PDCD4, inhibiting its transcription. Functional studies showed that miR-761 knockdown restored PDCD4 expression, increasing apoptosis and reducing proliferation and migration. Conversely, miR-761 overexpression enhanced these capacities in PDCD4-low cancer cells, effects reversed by PDCD4 upregulation. In vivo xenograft models demonstrated that miR-761 inhibition reduced tumor growth, with increased PDCD4 expression.</p> Conclusions <p>MiR-761 is a critical regulator of PDCD4, modulating laryngeal cancer progression through apoptosis inhibition and pro-metastatic signaling. Targeting the miR-761/PDCD4 axis offers a promising therapeutic strategy for laryngeal cancer management.</p>

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Role of microRNA-761 in modulating laryngeal cancer cell proliferation, metastasis, and apoptosis: regulation of PDCD4 as a key mechanism

  • 期刊论文

  • 发表日期：

    2025年10月17日

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  • Ruiqing Chen,
  • Zeng Wang,
  • Bing Wu,
  • Dangqing Liu,
  • Yuanteng Xu

摘要

Background

Laryngeal cancer is a leading global cause of cancer-related mortality. The regulatory interplay between dysregulated microRNA-761 (miR-761) and oncogenic signaling pathways in laryngeal carcinogenesis has not been fully elucidated‌.

Methods

This study explored the interaction between miR-761 and programmed cell death protein 4 (PDCD4) through dual-luciferase assay, cell proliferation and migration assays, and xenograft models.

Results

MiR-761 was significantly upregulated in laryngeal cancer tissues and cell lines, inversely correlating with PDCD4 downregulation. Computational predictions and dual-luciferase assays confirmed that miR-761 targets the 3’-UTR of PDCD4, inhibiting its transcription. Functional studies showed that miR-761 knockdown restored PDCD4 expression, increasing apoptosis and reducing proliferation and migration. Conversely, miR-761 overexpression enhanced these capacities in PDCD4-low cancer cells, effects reversed by PDCD4 upregulation. In vivo xenograft models demonstrated that miR-761 inhibition reduced tumor growth, with increased PDCD4 expression.

Conclusions

MiR-761 is a critical regulator of PDCD4, modulating laryngeal cancer progression through apoptosis inhibition and pro-metastatic signaling. Targeting the miR-761/PDCD4 axis offers a promising therapeutic strategy for laryngeal cancer management.