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RHAMM inhibits cell migration via the AKT/GSK3β/Snail axis in luminal A subtype breast cancer

Juan Wang1, Dan Li1, Wenzhi Shen2

  • 1Department of Anatomy and Histology, School of Medicine, Nankai University, Tianjin, China.

Anatomical Record (Hoboken, N.J. : 2007)
|November 27, 2019
PubMed

Insights

Receptor for hyaluronan mediated motility (RHAMM) inhibits cell migration in luminal A breast cancer by regulating the AKT/GSK3β/Snail pathway. This finding suggests RHAMM as a potential therapeutic target for breast cancer treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Breast cancer metastasis remains a significant challenge despite falling mortality rates.
  • Effective treatments to reduce breast cancer metastasis are still needed.
  • Understanding cell migration pathways is crucial for developing new therapies.

Purpose of the Study:

  • To investigate the role of Receptor for Hyaluronan Mediated Motility (RHAMM) in cell migration within luminal A breast cancer.
  • To identify the signaling pathway associated with RHAMM's function in this cancer subtype.
  • To explore RHAMM as a potential therapeutic target for breast cancer.

Main Methods:

  • Examined RHAMM expression in human breast tissues using microarrays.
  • Utilized in vitro (loss-of-function, gain-of-function) and in vivo models to study RHAMM's role in cell migration.
  • Investigated signaling molecules involved in cell migration using Western blot analysis.

Main Results:

  • RHAMM expression is elevated in malignant breast tissues.
  • RHAMM expression is lower in luminal A breast cancer compared to other subtypes.
  • RHAMM was found to inhibit, not promote, cell migration in luminal A breast cancer.
  • RHAMM inhibits cell migration through the AKT/GSK3β/Snail signaling axis.

Conclusions:

  • RHAMM plays a novel inhibitory role in cell migration in luminal A breast cancer.
  • The AKT/GSK3β/Snail pathway mediates RHAMM's inhibitory effect on cell migration.
  • RHAMM represents a potential therapeutic target for various breast cancer subtypes.
Keywords:
AKT/GSK3β/SnailRHAMMluminal A subtype

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