MicroRNA-224 modulates chemosensitivity of breast cancer cells to docetaxel by apoptosis inhibitor 5

J BUON. 2021 Mar-Apr;26(2):450-458.

Abstract

Purpose: The view that microRNA-224 (miR-224) may lead to tumorigenesis has been accepted in many studies. However, its role remains unclear in modulating the chemosensitivity of breast cancer cells to docetaxel (DOC). Thus, the aim of this study was to estimate what's the role of miR-224 in the chemosensitivity of breast cancer cells to DOC.

Methods: The role of miR-224 in breast cancer cells was analyzed using CCK-8 assay, real-time PCR, flow cytometry assay and Western blot. Dual-luciferase reporter assay and API-5-siRNA technology were performed to analyze the association between miR-224 and Apoptosis inhibitor 5 (API-5).

Results: Overexpression of miR-224 could significantly decrease the chemosensitivity of MCF-7 breast cancer cells to DOC. The luciferase activity of MCF-7/DOC cells containing wild-type 3'UTR of API-5 could be inhibited by miR-224 mimics. Similarly, the chemoresistance of MCF-7 cells to DOC induced by miR-224 mimics could be partially reversed by API-5-siRNA.

Conclusion: An inverse association between miR-224 and API-5 in breast cancer cells was revealed. Dysregulation of miR-224 plays a vital role in the acquired DOC resistance of breast cancer and at least partially via targeting API-5.

MeSH terms

  • Antineoplastic Agents / pharmacology
  • Antineoplastic Agents / therapeutic use*
  • Apoptosis / drug effects
  • Apoptosis Regulatory Proteins / metabolism*
  • Breast Neoplasms / drug therapy*
  • Breast Neoplasms / pathology
  • Docetaxel / pharmacology*
  • Female
  • Humans
  • MicroRNAs / metabolism*
  • Nuclear Proteins / metabolism*
  • Transfection

Substances

  • API5 protein, human
  • Antineoplastic Agents
  • Apoptosis Regulatory Proteins
  • MIRN224 microRNA, human
  • MicroRNAs
  • Nuclear Proteins
  • Docetaxel