Epigenetic control of the basal-like gene expression profile via Interleukin-6 in breast cancer cells

Mol Cancer. 2010 Nov 23:9:300. doi: 10.1186/1476-4598-9-300.

Abstract

Background: Basal-like carcinoma are aggressive breast cancers that frequently carry p53 inactivating mutations, lack estrogen receptor-α (ERα) and express the cancer stem cell markers CD133 and CD44. These tumors also over-express Interleukin 6 (IL-6), a pro-inflammatory cytokine that stimulates the growth of breast cancer stem/progenitor cells.

Results: Here we show that p53 deficiency in breast cancer cells induces a loss of methylation at IL-6 proximal promoter region, which is maintained by an IL-6 autocrine loop. IL-6 also elicits the loss of methylation at the CD133 promoter region 1 and of CD44 proximal promoter, enhancing CD133 and CD44 gene transcription. In parallel, IL-6 induces the methylation of estrogen receptor (ERα) promoter and the loss of ERα mRNA expression. Finally, IL-6 induces the methylation of IL-6 distal promoter and of CD133 promoter region 2, which harbour putative repressor regions.

Conclusion: We conclude that IL-6, whose methylation-dependent autocrine loop is triggered by the inactivation of p53, induces an epigenetic reprogramming that drives breast carcinoma cells towards a basal-like/stem cell-like gene expression profile.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • AC133 Antigen
  • Antigens, CD / genetics
  • Antigens, CD / metabolism
  • Blotting, Western
  • Breast Neoplasms / genetics*
  • Breast Neoplasms / metabolism*
  • Cell Line, Tumor
  • DNA Methylation / drug effects
  • DNA Methylation / genetics
  • DNA Methylation / physiology
  • Enzyme-Linked Immunosorbent Assay
  • Estrogen Receptor alpha / genetics
  • Estrogen Receptor alpha / metabolism
  • Female
  • Fluorescent Antibody Technique
  • Glycoproteins / genetics
  • Glycoproteins / metabolism
  • Humans
  • Hyaluronan Receptors / genetics
  • Hyaluronan Receptors / metabolism
  • Interleukin-6 / genetics
  • Interleukin-6 / metabolism*
  • Interleukin-6 / pharmacology
  • Peptides / genetics
  • Peptides / metabolism
  • RNA Interference
  • RNA, Messenger
  • Reverse Transcriptase Polymerase Chain Reaction
  • Tumor Suppressor Protein p53 / metabolism

Substances

  • AC133 Antigen
  • Antigens, CD
  • Estrogen Receptor alpha
  • Glycoproteins
  • Hyaluronan Receptors
  • Interleukin-6
  • PROM1 protein, human
  • Peptides
  • RNA, Messenger
  • Tumor Suppressor Protein p53