Gap Junctions and Breast Cancer Dormancy

Trends Cancer. 2020 Apr;6(4):348-357. doi: 10.1016/j.trecan.2020.01.013. Epub 2020 Feb 20.

Abstract

Breast cancer (BC) relapse, despite clinical advancement, remains one of the biggest issues in the field. Intercellular communication, specifically via connexin (Cx)-mediated gap junctions (GJs), play a key role in the long-term survival of these, treatment-resistant breast cancer stem cells (CSCs), allowing for relapse. Both basic and clinical evidence reveal dual roles for GJs, in tumor suppression, generally referred to as dormancy, and progression and metastasis. GJ intercellular communication (GJIC) can be mediated by multiple types of Cxs, depending on the organ to which the BC cells metastasize. This review expands on the differential expression of Cx-mediated GJIC between CSCs and niche cells within a given microenvironment.

Keywords: bone marrow; breast cancer; connexin; dormancy; gap junction; metastasis.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Antineoplastic Agents / pharmacology
  • Antineoplastic Agents / therapeutic use
  • Autophagy / drug effects
  • Autophagy / immunology
  • Breast / growth & development
  • Breast / pathology
  • Breast Neoplasms / drug therapy
  • Breast Neoplasms / immunology
  • Breast Neoplasms / pathology*
  • Cell Communication / drug effects
  • Cell Communication / immunology
  • Connexins / antagonists & inhibitors
  • Connexins / drug effects
  • Connexins / immunology
  • Connexins / metabolism*
  • Disease Models, Animal
  • Drug Resistance, Neoplasm / drug effects
  • Drug Resistance, Neoplasm / immunology
  • Female
  • Gap Junctions / drug effects
  • Gap Junctions / immunology
  • Gap Junctions / pathology*
  • Humans
  • Mammary Glands, Animal / growth & development
  • Mammary Glands, Animal / pathology
  • Mice
  • Neoplasm Recurrence, Local / immunology
  • Neoplasm Recurrence, Local / pathology*
  • Neoplasm Recurrence, Local / prevention & control
  • Neoplastic Stem Cells / pathology
  • Tumor Escape / drug effects
  • Tumor Microenvironment / drug effects
  • Tumor Microenvironment / immunology

Substances

  • Antineoplastic Agents
  • Connexins