Copyright © 2007 Cell Press. All rights reserved.
Cancer Cell, Vol 12, 252-265, 11 September 2007
Article
Human C-Reactive Protein Binds Activating Fcγ Receptors and Protects Myeloma Tumor Cells from Apoptosis
1 Department of Lymphoma and Myeloma, Division of Cancer Medicine, and the Center for Cancer Immunology Research, The University of Texas M.D. Anderson Cancer Center, Houston, TX 77030, USA
2 Department of Hematopathology, Division of Pathology, and Laboratory Medicine, The University of Texas M.D. Anderson Cancer Center, Houston, TX 77030, USA
3 State Key Laboratory of Genetics, Institute of Genetics, School of Life Science, Fudan University, Shanghai 200433, China
∗Corresponding author
Qing Yi
qyi@mdanderson.org
Summary
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 Fcγ receptors; activates PI3K/Akt, ERK, and NF-κB 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.
