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Updated: Aug 1, 2026

Profiling of Estrogen-regulated MicroRNAs in Breast Cancer Cells
16:24

Profiling of Estrogen-regulated MicroRNAs in Breast Cancer Cells

Published on: February 21, 2014

The "good-cop bad-cop" TGF-beta role in breast cancer modulated by non-coding RNAs

Diana Gulei1, Nikolay Mehterov2, Hui Ling3

  • 1MEDFUTURE-Research Center for Advanced Medicine, University of Medicine and Farmacy Iuliu-Hatieganu, Marinescu 23 Street, Cluj-Napoca, Romania.

Biochimica Et Biophysica Acta. General Subjects
|April 16, 2017
PubMed
Abstract

Insights

Transforming growth factor beta (TGFβ)-induced epithelial-mesenchymal transition (EMT) drives breast cancer progression and drug resistance. Understanding non-coding RNA regulation of EMT is key to developing new targeted therapies.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Lack of early diagnosis and drug resistance increase breast cancer mortality.
  • TGFβ-induced epithelial-mesenchymal transition (EMT) promotes cancer cell migration, invasion, and chemoresistance.
  • TGFβ shifts from a tumor suppressor to an oncogene, fostering a pro-tumorigenic microenvironment.

Purpose of the Study:

  • To review updated knowledge on TGFβ-induced EMT in breast cancer.
  • To highlight the regulatory roles of non-coding RNAs, including miR-200 family and HOTAIRM1.
  • To present the phenotype P-EMT and its complex feedback loops with key regulatory molecules.

Main Methods:

  • Comprehensive literature review of recent data on TGFβ-induced EMT.
  • Focus on non-coding RNA involvement (miR-200, HOTAIRM1).
  • Analysis of P-EMT phenotype and associated regulatory networks.

Main Results:

  • EMT is linked to aggressive breast cancer and poor patient survival.
  • EMT facilitates drug resistance, invasion, and metastasis.
  • Non-coding RNAs significantly modulate TGFβ-induced EMT.

Conclusions:

  • Inhibiting EMT is a potential therapeutic strategy for breast cancer.
  • Understanding non-coding RNA roles in EMT can lead to novel targeted treatments.
  • This review consolidates current data to inform future therapeutic development.
Keywords:
Breast cancerEMTTGF-βlncRNAmiRNA

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