Human C-reactive protein binds activating Fcgamma receptors and protects myeloma tumor cells from apoptosis

Cancer Cell. 2007 Sep;12(3):252-65. doi: 10.1016/j.ccr.2007.08.008.


Elevated levels of C-reactive protein (CRP) are present in many disease situations including malignancies and may contribute to the pathogenesis of cardiovascular disorders. This study was undertaken in a myeloma setting to determine whether CRP affects tumor cell growth and survival. We show that CRP enhanced myeloma cell proliferation under stressed conditions and protected myeloma cells from chemotherapy drug-induced apoptosis in vitro and in vivo. CRP binds activating Fcgamma receptors; activates PI3K/Akt, ERK, and NF-kappaB pathways; and inhibits caspase cascade activation induced by chemotherapy drugs. CRP also enhanced myeloma cell secretion of IL-6 and synergized with IL-6 to protect myeloma cells from chemotherapy drug-induced apoptosis. Thus, our results implicate CRP as a potential target for cancer treatment.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / physiology*
  • C-Reactive Protein / physiology*
  • Cell Line, Tumor
  • Cell Proliferation
  • Humans
  • Interleukin-6 / metabolism
  • Mice
  • Multiple Myeloma / metabolism*
  • Multiple Myeloma / pathology
  • Receptors, IgG / metabolism*
  • Signal Transduction


  • Interleukin-6
  • Receptors, IgG
  • C-Reactive Protein