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Updated: Dec 18, 2025

Isolation and Functional Assessment of Human Breast Cancer Stem Cells from Cell and Tissue Samples
07:03

Isolation and Functional Assessment of Human Breast Cancer Stem Cells from Cell and Tissue Samples

Published on: October 2, 2020

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Caveolin-1 inhibits breast cancer stem cells via c-Myc-mediated metabolic reprogramming

Shengqi Wang1,2,3, Neng Wang1,3,4, Yifeng Zheng1,2,3

  • 1Integrative Research Laboratory of Breast Cancer, the Research Center for Integrative Cancer Medicine, Discipline of Integrated Chinese and Western Medicine & the Second Clinical College of Guangzhou University of Chinese Medicine, Guangzhou, 510006, China.

Cell Death & Disease
|June 13, 2020
PubMed

Insights

Downregulation of Caveolin-1 (Cav-1) in breast cancer stem cells (BCSCs) promotes aerobic glycolysis and tumor growth. Restoring Cav-1 may offer a new strategy for BCSC elimination and improved patient survival.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Metabolism

Background:

  • Breast cancer stem cells (BCSCs) drive tumor initiation and progression.
  • Understanding BCSC metabolism is crucial for developing targeted therapies.
  • Current knowledge of BCSC metabolic regulation remains limited.

Purpose of the Study:

  • To investigate the role of Caveolin-1 (Cav-1) in regulating BCSC metabolism.
  • To elucidate the molecular mechanisms underlying Cav-1's function in BCSCs.
  • To assess the therapeutic potential of targeting Cav-1 for BCSC elimination.

Main Methods:

  • Analysis of Cav-1 expression in BCSCs.
  • Metabolic assays to evaluate mitochondrial respiration and aerobic glycolysis.
  • Studies in transgenic mice to assess tumor formation and progression.
  • Investigation of the proteasome pathway and c-Myc regulation.

Main Results:

  • Downregulation of Cav-1 in BCSCs correlates with a metabolic shift towards aerobic glycolysis.
  • Cav-1 inhibits BCSC self-renewal and aerobic glycolysis.
  • Cav-1 loss accelerates mammary tumor development in mice, associated with increased BCSC activity.
  • Cav-1 promotes c-Myc degradation via VHL-mediated ubiquitination and proteasomal pathways.
  • Epithelial Cav-1 expression in patients is linked to better survival and delayed onset.

Conclusions:

  • Cav-1 plays a critical role in regulating BCSC metabolism and function.
  • Cav-1 downregulation promotes a pro-tumorigenic metabolic phenotype in BCSCs.
  • Targeting Cav-1 presents a promising therapeutic strategy for breast cancer treatment by eliminating BCSCs.

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