IL-4-mediated drug resistance in colon cancer stem cells

Cell Cycle. 2008 Feb 1;7(3):309-13. doi: 10.4161/cc.7.3.5389. Epub 2007 Nov 30.


Cancer stem cells are defined as cells able to both extensively self-renew and differentiate into progenitors. Cancer stem cells are thus likely to be responsible for maintaining or spreading a cancer, and may be the most relevant targets for cancer therapy. The CD133 glycoprotein was recently described as a reliable cancer stem-like cell marker in colon carcinoma. CD133+ cells are both necessary and sufficient to initiate tumour growth in animal models. The CD133+ cell population and spheroid cultures contain cells expressing the stem cell marker Musashi-1 which is involved in maintenance of stem cell fate in several tissues and importantly, this expression is maintained in stem-like cells derived from xenografted tumors. Here we discuss the potential use of the CD133 antigen in concert with Musashi-1 as markers to identify the colon cancer stem cell population. Since the upregulation of IL-4 cytokine was recently demonstrated to constitute an important mechanism that protects the tumorigenic CD133+ cells from apoptosis, the potential benefits of standard chemotherapeutic treatments in combination with IL-4 inhibitors in the context of human colon carcinoma, are also discussed.

Publication types

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

MeSH terms

  • Animals
  • Antineoplastic Agents / pharmacology
  • Antineoplastic Agents / therapeutic use
  • Colonic Neoplasms / drug therapy
  • Colonic Neoplasms / genetics
  • Colonic Neoplasms / metabolism*
  • Drug Resistance, Neoplasm / drug effects
  • Drug Resistance, Neoplasm / physiology*
  • Humans
  • Interleukin-4 / genetics
  • Interleukin-4 / physiology*
  • Neoplastic Stem Cells / physiology*


  • Antineoplastic Agents
  • Interleukin-4