Research Highlights

• Subject Category:
  • Cell & molecular biology

Published online: 10 January 2008 | doi:10.1038/nchina.2007.289

Breast cancer: Destroying bad seeds

Wei Zeng

Introduction

Cancer stem cells are thought to be the 'bad seeds' of cancer. They are the only cells capable of giving rise to new tumours and are resistant to chemotherapy. Destroying cancer stem cells could potentially block cancer development. Erwei Song at Sun Yat-sen University in Guangzhou, Judy Lieberman at Harvard Medical School and co-workers¹ showed that breast-cancer stem cells could be blocked from self-renewal and differentiation through the interference of let-7 microRNAs.

The researchers first screened for microRNAs (single stranded RNA molecules) that regulate the development of breast-cancer stem cells. They found that let-7, a known tumour-suppressing microRNA, was significantly and consistently reduced in cancer stem cells. Observations in vitro showed that when the let-7 level was high, cell division decreased and the majority of stem cells underwent irreversible differentiation, thus ceasing to be stem cells. Tumour growth was also found to be suppressed in vivo. When the let-7 level was low, non-stem cancer cells could self-renew in vitro. In addition the researchers found that let-7 regulates the division and differentiation of breast-cancer stem cells by silencing H-RAS and HMGA2 genes, respectively.

The findings suggest that the interference of let-7 could block breast-cancer stem cells from self-renewal and differentiation, which points to a new direction for future breast-cancer therapy.

The authors of this work are from:
Department of Breast Surgery, No. 2 Affiliated Hospital, Sun Yat-sen University, Guangzhou, China; Immune Disease Institute, Harvard Medical School, Boston, Massachusetts, USA; Department of Pharmacology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.

Reference

1. Yu, F. et al. let-7 regulates self renewal and tumorigenicity of breast cancer cells. Cell 131, 1109–1123 (2007). | Article | PubMed |