Reawakening the master switches in triple-negative breast cancer: A strategic blueprint for confronting metastasis and chemoresistance via microRNA-200/205: A systematic review

Crit Rev Oncol Hematol. 2024 Dec:204:104516. doi: 10.1016/j.critrevonc.2024.104516. Epub 2024 Sep 19.

Abstract

Triple-negative breast cancer (TNBC) exhibits a proclivity for early recurrence and development of metastasis. Moreover, drug resistance tends to arise few months following chemotherapeutic regimen with agents such as Doxorubicin, Paclitaxel, Docetaxel, and Cisplatin. miR-200 family and miR-205 are considered key regulators of metastasis by regulating the Epithelial-to-mesenchymal transition (EMT) via inhibiting ZEB1. Therefore, these microRNAs may offer therapeutic applications. Moreover, they hold potential for inhibiting chemoresistance and increasing chemosensitivity. These microRNAs are suppressed in TNBC cells. Increasing their levels, however, can inhibit EMT and improve progression-free survival (PFS). Besides using direct miRNA therapy via viral vectors, some drugs like Acetaminophen, or Tamoxifen are deemed useful for TNBC due to their ability to upregulate these miRNAs. In this review, by conducting an advanced search on PubMed, Embase, and Medline and selecting pertinent studies, we aimed to explore the potential applications of these microRNAs in controlling EMT and overcoming chemoresistance.

Keywords: Chemotherapy resistance; Metastasis; TNBC; Triple-negative; miRNA-200; miRNA-205.

Publication types

  • Systematic Review
  • Review

MeSH terms

  • Drug Resistance, Neoplasm* / genetics
  • Epithelial-Mesenchymal Transition* / drug effects
  • Epithelial-Mesenchymal Transition* / genetics
  • Female
  • Gene Expression Regulation, Neoplastic / drug effects
  • Humans
  • MicroRNAs* / genetics
  • Neoplasm Metastasis*
  • Triple Negative Breast Neoplasms* / drug therapy
  • Triple Negative Breast Neoplasms* / genetics
  • Triple Negative Breast Neoplasms* / pathology

Substances

  • MicroRNAs
  • MIRN200 microRNA, human
  • MIRN205 microRNA, human