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  2. Down-regulation Of Mir-125b By Hpv16 E6 Might Promote Cervical Cancer Progression Through Taz/tead.
  1. Home
  2. Down-regulation Of Mir-125b By Hpv16 E6 Might Promote Cervical Cancer Progression Through Taz/tead.

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Down-regulation of miR-125b by HPV16 E6 might promote cervical cancer progression through TAZ/TEAD.

Yongli Hou1, Lili Zhang1, Wenhao Wang1

  • 1Department of Gynecology and Obstetrics, The Second Hospital of Shanxi Medical University, Taiyuan, Shanxi, China.

Frontiers in Oncology
|April 30, 2025

View abstract on PubMed

Summary
This summary is machine-generated.

MicroRNA-125b (miR-125b) is downregulated by HPV16 E6 in cervical cancer, inhibiting cell proliferation and migration by targeting TAZ. MiR-125b is a potential therapeutic target for HPV-induced cervical cancer.

Keywords:
HPV16 E6Hippo pathwayTAZcervical cancermiR-125b

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Area of Science:

  • Oncology
  • Molecular Biology
  • Virology

Background:

  • MicroRNA (miRNA) dysregulation is implicated in cancer development.
  • Human papillomavirus type 16 (HPV16) is a major cause of cervical cancer.
  • The role of miR-125b in HPV16-driven cervical cancer progression via TAZ needs investigation.

Purpose of the Study:

  • To investigate the role of miR-125b in HPV16-positive cervical cancer.
  • To determine if miR-125b regulates cervical cancer biological behaviors through TAZ.
  • To explore miR-125b as a potential therapeutic target.

Main Methods:

  • Bioinformatics analysis identified differentially expressed miRNAs.
  • Quantitative reverse transcription PCR (RT-qPCR) measured miR-125b expression in patient tissues and cell lines.
  • Dual-luciferase reporter assays assessed the miR-125b-TAZ interaction.
  • Functional assays (mimic/inhibitor) evaluated miR-125b effects on cell proliferation, migration, invasion, and apoptosis.
  • Western blot analysis assessed protein expression.
  • Main Results:

    • miR-125b expression was significantly reduced in high-grade squamous intraepithelial lesion (HSIL) and cervical squamous cell carcinoma compared to normal tissue.
    • miR-125b mimic inhibited SiHa cell proliferation, migration, and invasion, enhancing apoptosis, with decreased HPV16 E6, TAZ, and TEAD mRNA.
    • HPV16 E6 overexpression suppressed miR-125b and enhanced TAZ and TEAD expression.

    Conclusions:

    • HPV16 E6 downregulates miR-125b, promoting cervical cancer progression by targeting TAZ and regulating the Hippo pathway.
    • miR-125b acts as a tumor suppressor in HPV-induced cervical cancer.
    • miR-125b represents a promising therapeutic target for cervical cancer.