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FOXM1 Promotes Drug Resistance in Cervical Cancer Cells by Regulating ABCC5 Gene Transcription

Youxiang Hou1, Zhanfei Dong2, Wei Zhong1

  • 1Department of Radiation Oncology, The Affiliated Cancer Hospital of Xinjiang Medical University, 789 Suzhou Dong Jie, Xinshi District, Urumqi, Xinjiang 86830000, China.

Biomed Research International
|February 10, 2022
PubMed
Abstract

Insights

Forkhead box M1 (FOXM1) drives paclitaxel resistance in cervical cancer by upregulating ABCC5. Inhibiting FOXM1 enhances paclitaxel

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Cervical cancer treatment often involves paclitaxel chemotherapy.
  • Drug resistance significantly limits the efficacy of paclitaxel in cervical cancer.
  • Identifying mechanisms of resistance is crucial for developing effective therapies.

Purpose of the Study:

  • To investigate the role of forkhead box M1 (FOXM1) in paclitaxel resistance in cervical cancer cells.
  • To elucidate the molecular mechanisms underlying FOXM1-mediated drug resistance.
  • To identify potential therapeutic targets for overcoming paclitaxel resistance.

Main Methods:

  • Establishment of paclitaxel-resistant Caski cells (Caski/Taxol).
  • Overexpression and knockdown of FOXM1 to assess its effect on drug resistance.
  • Measurement of protein and mRNA levels of FOXM1 and ABCC5.
  • Analysis of cell apoptosis, migration, and intracellular paclitaxel concentrations.

Main Results:

  • Paclitaxel-resistant cells exhibited higher expression of FOXM1 and ABCC5.
  • Knockdown of FOXM1 reduced FOXM1 and ABCC5 levels, increasing intracellular paclitaxel.
  • FOXM1 knockdown promoted paclitaxel-induced apoptosis in resistant cells.

Conclusions:

  • FOXM1 promotes paclitaxel resistance in cervical cancer by regulating ABCC5 gene transcription.
  • Targeting FOXM1, potentially via shRNA or Siomycin A, can enhance paclitaxel efficacy.
  • FOXM1 is a promising therapeutic target for overcoming drug resistance in cervical cancer.

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