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Prolactin modulates TNBC aggressive phenotype limiting tumorigenesis

Vanessa M López-Ozuna1, Ibrahim Y Hachim1, Mahmood Y Hachim2

  • 1Department of Medicine, Cancer Research Program, McGill University Health Centre, McGill University, Montreal, Québec, Canada.

Endocrine-Related Cancer
|January 15, 2019
PubMed

Insights

The lactogenic hormone prolactin (PRL) depletes aggressive breast cancer stem cells in triple-negative breast cancer (TNBC). This reprogramming induces differentiation, reduces tumor growth, and offers a potential new therapeutic strategy for TNBC.

Area of Science:

  • Oncology
  • Cell Biology
  • Endocrinology

Background:

  • Triple-negative breast cancer (TNBC) is aggressive and lacks targeted therapies.
  • TNBC is characterized by poor differentiation and enrichment of cancer stem-like cells (CSCs).
  • Breast cancer stem-like cells (BCSCs) drive tumor aggressiveness and recurrence.

Purpose of the Study:

  • To investigate the effect of prolactin (PRL) on BCSCs in TNBC.
  • To explore PRL's potential as a therapeutic agent for TNBC.

Main Methods:

  • Treatment of TNBC cells with PRL.
  • Analysis of BCSC subpopulations (CD44+/CD24-, ALDH+).
  • Assessment of tumorsphere formation and self-renewal capacity.
  • Histological and molecular analysis of cellular differentiation and senescence (H3K9me3).
  • In vivo evaluation in a TNBC xenograft mouse model.

Main Results:

  • PRL treatment significantly depleted CD44+/CD24- and ALDH+ BCSCs.
  • PRL induced differentiation towards a less tumorigenic phenotype (CD44-/CD24-, ALDH-).
  • PRL treatment limited tumorsphere formation and self-renewal capacity.
  • PRL induced a heterochromatin phenotype (H3K9me3) associated with differentiation and senescence.
  • PRL controlled tumor growth in a pre-clinical TNBC xenograft model.

Conclusions:

  • PRL exerts anti-tumorigenic effects on TNBC by depleting BCSCs.
  • PRL promotes cellular reprogramming and differentiation in TNBC cells.
  • PRL's effects on BCSCs and tumor growth suggest potential therapeutic applications for TNBC.
Keywords:
cellular plasticityepigenetics regulationstem cell differentiationxenografts

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