Interleukin-6 and prostate cancer progression

Cytokine Growth Factor Rev. 2001 Mar;12(1):33-40. doi: 10.1016/s1359-6101(00)00021-6.


Prostate cancer, while initially dependent on androgens for proliferation, progresses to an androgen-independent state. Evidence has been accumulating that interleukin-6 (IL-6) may contribute to prostate cancer progression. Serum levels of IL-6 correlate with prostate tumor burden and patient morbidity. The prostate tissue itself appears to be a source of IL-6 and its receptor. Furthermore, experimental data suggest that IL-6 is an autocrine and paracrine growth factor for androgen-independent prostate cancer cell lines. For example, inhibition of IL-6, with anti-IL-6 antibody, sensitizes androgen-independent prostate cancer cells to chemotherapeutic agents in vitro. Finally, IL-6 activates a variety of signal transduction cascades, some which stimulate androgen receptor activity, in prostate cancer cells. These data suggest that targeting IL-6 may have multiple benefits in prostate cancer patients.

Publication types

  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Animals
  • Humans
  • Interleukin-6 / analysis
  • Interleukin-6 / metabolism*
  • Interleukin-6 / pharmacology
  • Male
  • Prostatic Neoplasms / drug therapy
  • Prostatic Neoplasms / metabolism*
  • Prostatic Neoplasms / physiopathology
  • Receptors, Androgen / metabolism
  • Receptors, Interleukin-6 / analysis
  • Receptors, Interleukin-6 / metabolism
  • Signal Transduction
  • Tumor Cells, Cultured


  • Interleukin-6
  • Receptors, Androgen
  • Receptors, Interleukin-6