p52-Independent nuclear translocation of RelB promotes LPS-induced attachment.
The NF-kappaB 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-kappaB 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 beta1 integrin expression and cellular attachment through an NF-kappaB-dependent mechanism. Blocking RelB expression prevented the increase in the expression of beta1 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.
Saito
T
T
Laboratory of Immunology, National Institute on Aging, NIH Biomedical Research Center, Baltimore, MD 21224, USA.
Sasaki
C Y
CY
Rezanka
L J
LJ
Ghosh
P
P
Longo
D L
DL
D021581:Active Transport, Cell Nucleus; D002448:Cell Adhesion; D045744:Cell Line, Tumor; D002467:Cell Nucleus / Q000378:metabolism*; D006801:Humans; D019012:Integrin beta1 / Q000096:biosynthesis; D008070:Lipopolysaccharides / Q000276:immunology; D008175:Lung Neoplasms / Q000276:immunology / Q000378:metabolism / Q000473:pathology*; D052003:NF-kappa B p52 Subunit / Q000378:metabolism*; D055752:Small Cell Lung Carcinoma / Q000276:immunology / Q000378:metabolism / Q000473:pathology*; D051841:Transcription Factor RelB / Q000378:metabolism*
D019012:Integrin beta1; D008070:Lipopolysaccharides; D052003:NF-kappa B p52 Subunit; D051841:Transcription Factor RelB