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EPAS1 targeting by miR-152-3p in Paclitaxel-resistant Breast Cancer.

Ying Song1, Mo Zhang2, Man Man Lu1

  • 1Department of Pathology, Xinxiang Medical University, Xinxiang, Henan 453003, P.R. China.

Journal of Cancer
|September 11, 2020
PubMed
Summary

MicroRNA-152-3p (miR-152-3p) enhances paclitaxel sensitivity in breast cancer by targeting EPAS1. This microRNA reduces cancer cell survival and promotes apoptosis, overcoming drug resistance.

Keywords:
Breast cancerEPAS1Paclitaxeldrug resistancemiR-152-3p

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Area of Science:

  • Molecular Biology
  • Oncology
  • Biochemistry

Background:

  • Paclitaxel is crucial for breast cancer chemotherapy, but drug resistance remains a significant challenge.
  • MicroRNA-152-3p (miR-152-3p) is implicated in tamoxifen resistance; its role in paclitaxel resistance is unexplored.

Purpose of the Study:

  • To investigate the role of miR-152-3p in paclitaxel resistance in breast cancer.
  • To identify and validate the target gene of miR-152-3p involved in this resistance mechanism.

Main Methods:

  • Quantitative real-time PCR (qRT-PCR) to assess miR-152-3p expression in breast cancer tissues and cells.
  • Cell viability (MTT assay) and apoptosis (flow cytometry) analyses in paclitaxel-resistant MCF-7/TAX cells transfected with miR-152-3p mimics.
  • Bioinformatics analysis and dual-luciferase reporter assays to identify and confirm EPAS1 as the miR-152-3p target.
  • RNA interference (siRNA) to investigate the functional role of EPAS1 in paclitaxel resistance.

Main Results:

  • miR-152-3p expression was significantly lower in breast cancer tissues and cells compared to normal controls.
  • Overexpression of miR-152-3p in MCF-7/TAX cells reduced cell survival, increased apoptosis, and enhanced sensitivity to paclitaxel.
  • Endothelial PAS domain-containing protein 1 (EPAS1) was confirmed as a direct target gene negatively regulated by miR-152-3p.
  • Silencing EPAS1 expression mimicked the effects of miR-152-3p overexpression, increasing paclitaxel sensitivity and apoptosis.

Conclusions:

  • miR-152-3p enhances breast cancer cell sensitivity to paclitaxel by targeting and downregulating EPAS1 expression.
  • This mechanism involves inhibiting cell survival and promoting apoptosis in paclitaxel-resistant cells.
  • miR-152-3p represents a potential therapeutic target for overcoming paclitaxel resistance in breast cancer.