4.6 Article

p52-independent nuclear translocation of RelB promotes LPS-induced attachment

Journal

Publisher

ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2009.11.039

Keywords

LPS; SCLC; NF-kappa B; p65; p52; RelB; Cellular attachment; beta 1 integrin

Funding

  1. National Institutes of Health, National Institute on Aging
  2. NATIONAL INSTITUTE ON AGING [ZIGAG000621, ZIAAG000426] Funding Source: NIH RePORTER

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The NF-kappa B signaling pathways have a critical role in the development and progression of various cancers In this study. we demonstrated that the small Cell lung cancer cell line (SCLC) H69 expressed a unique NF-kappa B profile as compared to other cancer cell lines The p105/p50, p100/p52, c-Rel, and RelB protein and mRNA transcripts were absent in H69 cells but these cells expressed RelA/p65 The activation of H69 cells by lipopolysaccharide (LPS) resulted in the induction of RelB and p100 expression The treatment also induced the nuclear translocation of RelB without the processing of p100 to p52 Furthermore, LPS-induced beta 1 integrin expression and Cellular attachment through an NF-kappa B-dependent mechanism Blocking RelB expression prevented the increase in the expression of beta 1 integrin and the attachment of H69 Taken together, the results Suggest that RelB was responsible for the LPS-mediated attachment and may play an important role in the progression of some cancers Published by Elsevier Inc

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