Linked Life Data

18644982

Source:http://linkedlifedata.com/resource/pubmed/id/18644982

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
2008-7-22
pubmed:abstractText
The small GTPase Rac1 can stimulate various signaling pathways that contribute to cell transformation. In particular, the activation of the NFkappaB transcription factor initiates an antiapoptotic response and promotes cell cycle progression through increased cyclin D1 expression. As a potential oncogenic mechanism to up-regulate this pathway, the overexpression of the Rac1b splicing variant was reported in some colorectal tumors. Rac1b exists predominantly in the active GTP-bound state and selectively promotes the pathway leading to NFkappaB activation. Here, we studied the role of endogenous Rac1b in colorectal cancer cells. We found that depletion of Rac1b by small interfering RNAs inhibited endogenous NFkappaB activation and reduced cell viability to 50% within 48 hours. This reduction was due to increased apoptosis, although a reduced G(1)-S progression rate was also observed. These data show, for the first time, that colorectal cells expressing alternative spliced Rac1b also depend on Rac1b signaling to sustain their survival.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
1541-7786
pubmed:author
pubmed:issnType
Print
pubmed:volume
6
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1178-84
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Increased Rac1b expression sustains colorectal tumor cell survival.
pubmed:affiliation
Centre of Human Genetics, National Health Institute Dr. Ricardo Jorge, Lisbon, Portugal.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't