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Title: Inhibition of NF-{kappa}B1 and NF-{kappa}B2 activation in prostate cancer cells treated with antibody against the carboxyl terminal domain of GRP78: Effect of p53 upregulation

Journal Article · · Biochemical and Biophysical Research Communications
 [1];  [2]
  1. Department of Pathology, Duke University Medical Center, Durham, NC 27710 (United States)
  2. BioResource International, Research Triangle Park, NC 27709 (United States)

Ligation of cancer cell surface GRP78 by activated {alpha}{sub 2}-macroglobulin ({alpha}{sub 2}M{sup *}) triggers pro-proliferative and anti-apoptotic signaling pathways. Cancer patients who develop autoantibodies to the {alpha}{sub 2}M{sup *} binding site in GRP78 have a poor prognosis since these antibodies are receptor agonists. The NF-{kappa}B family of transcription factors induces expression of genes affecting cell growth and differentiation. NF-{kappa}B1 plays a major regulatory role in controlling innate immunity and inflammation, whereas NF-{kappa}B2 plays a greater role in cancer cell proliferation. Here we report that treatment of prostate cancer cells with antibody directed against the carboxyl terminal domain of GRP78 inhibits {alpha}{sub 2}M{sup *}-induced activation of NF-{kappa}B2 by {approx}50% while exerting a lesser effect of {approx}20% on NF-{kappa}B1 activation. Treatment of these cells nearly abolished {alpha}{sub 2}M{sup *}-induced activation of IKK{alpha} involved in the activation of NF-{kappa}B2. This antibody also suppressed {alpha}{sub 2}M{sup *}-induced phosphorylation of IKK{alpha}, IKK{alpha}/{beta}, I{kappa}B{alpha}, and I{kappa}B{beta} as well as levels of NIK. Antibody treatment of cancer cells elevated pro-apoptotic p21WAF and p27kip while reducing cyclin D1 levels. These studies demonstrate that antibody directed against the carboxyl terminal domain of GRP78 inhibits the pro-proliferative NF-{kappa}B signaling cascade in cancer cells.

OSTI ID:
22202384
Journal Information:
Biochemical and Biophysical Research Communications, Vol. 392, Issue 4; Other Information: Copyright (c) 2010 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
Country of Publication:
United States
Language:
English