MiR-26a/miR-26b represses tongue squamous cell carcinoma progression by targeting PAK1

Zhenxing Wei1, Kunpeng Chang1, Chongsheng Fan1

  • 1Department of Otorhinolaryngology-Head and Neck Surgery, The Luoyang Central Hospital Affiliated to Zhengzhou University, No. 288 Middle Zhongzhou Road, Xigong District, Luoyang, 471000 Henan China.

Abstract

Insights

MicroRNA (miR)-26a and miR-26b suppress tongue squamous cell carcinoma (TSCC) progression by targeting p21 Activated Kinase 1 (PAK1). Restoring these microRNAs inhibits tumor growth, offering new therapeutic strategies for TSCC.

Area of Science:

  • Molecular Oncology
  • Cancer Biology
  • MicroRNA Therapeutics

Background:

  • Tongue squamous cell carcinoma (TSCC) is a prevalent oral malignancy.
  • Previous research indicated reduced expression of microRNA (miR)-26a and miR-26b in TSCC tissues.

Purpose of the Study:

  • To investigate the impact of miR-26a and miR-26b on TSCC progression.
  • To elucidate the underlying molecular mechanisms involving p21 Activated Kinase 1 (PAK1).

Main Methods:

  • Quantitative polymerase chain reaction (RT-qPCR) and western blotting to assess miR-26a, miR-26b, and PAK1 expression.
  • Flow cytometry for cell cycle and apoptosis analysis.
  • Transwell assays for cell migration and invasion.
  • Dual-luciferase reporter and RNA immunoprecipitation (RIP) assays to confirm miR-26a/miR-26b and PAK1 interaction.
  • In vivo studies using a xenograft tumor model.

Main Results:

  • miR-26a and miR-26b were underexpressed, while PAK1 was highly expressed in TSCC.
  • Overexpression of miR-26a/miR-26b suppressed TSCC cell proliferation, migration, invasion, and glycolysis, while enhancing apoptosis.
  • miR-26a/miR-26b directly targeted and downregulated PAK1; PAK1 introduction partially reversed these effects.
  • Restoration of miR-26a/miR-26b inhibited TSCC tumor growth in vivo.

Conclusions:

  • miR-26a and miR-26b act as tumor suppressors in TSCC by targeting PAK1.
  • These findings enhance the understanding of TSCC pathogenesis.
  • miR-26a/miR-26b represent potential therapeutic targets for TSCC treatment.

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