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Suppressive role exerted by microRNA-29b-1-5p in triple negative breast cancer through SPIN1 regulation

Rosa Drago-Ferrante1, Francesca Pentimalli2, Daniela Carlisi3

  • 1Laboratory of Biochemistry, Department of Biological, Chemical and Pharmaceutical Sciences and Technologies, University of Palermo, Polyclinic, Palermo, Italy.

Oncotarget
|April 21, 2017
PubMed

Insights

MicroRNA-29b-1-5p (miR-29b-1-5p) is downregulated in aggressive triple-negative breast cancer (TNBC). Restoring miR-29b-1-5p suppresses TNBC growth, stemness, and paclitaxel resistance by targeting SPINDLIN1 (SPIN1).

Area of Science:

  • Molecular Oncology
  • Cancer Stem Cell Biology
  • Gene Regulation

Background:

  • Dysregulation of the miR-29 family is implicated in various cancers, including breast cancer.
  • Triple-negative breast cancer (TNBC) is an aggressive subtype with limited therapeutic options.
  • Cancer stem cells (CSCs) contribute to tumor initiation, progression, and treatment resistance in TNBC.

Purpose of the Study:

  • To investigate the functional role of miR-29b-1 in human triple-negative breast cancer (TNBC).
  • To determine the correlation between miR-29b-1-5p expression and TNBC stem cell potential.
  • To elucidate the molecular mechanisms underlying miR-29b-1's tumor-suppressive functions in TNBC.

Main Methods:

  • Quantitative real-time PCR to assess miR-29b-1-5p expression in TNBC tissues and cell lines.
  • Mammosphere assays to evaluate cancer stem cell enrichment and self-renewal capacity.
  • Western blotting and luciferase reporter assays to confirm target gene interactions (SPIN1) and pathway analysis (WNT/β-catenin, AKT).

Main Results:

  • miR-29b-1-5p was significantly downregulated in human TNBC tissues and cell lines.
  • Reduced miR-29b-1-5p expression correlated with increased mammosphere formation and stemness gene (OCT4, NANOG, SOX2) enrichment.
  • Ectopic miR-29b-1-5p overexpression suppressed TNBC cell growth, self-renewal, migration, invasiveness, and paclitaxel resistance, partly via repression of SPINDLIN1 (SPIN1) and WNT/AKT pathways.

Conclusions:

  • miR-29b-1 deregulation contributes to multiple oncogenic features and renewal potential in TNBC cells.
  • The tumor-suppressive role of miR-29b-1-5p is mediated, at least partly, through the regulation of SPINDLIN1 (SPIN1).
  • miR-29b-1 and SPINDLIN1 represent potential novel therapeutic targets for TNBC treatment.
Keywords:
MiR-29b-1SPIN1Wnt/β-catenin and Akt signaling pathwayscancer stem cellstriple-negative breast cancer

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