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Role of CSN5/JAB1 in Wnt/β‐catenin activation in colorectal cancer cells
Author(s) -
Schütz Anke K.,
Hennes Thomas,
Jumpertz Sandra,
Fuchs Simone,
Bernhagen Jürgen
Publication year - 2012
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2012.04.037
Subject(s) - cop9 signalosome , colorectal cancer , wnt signaling pathway , protein subunit , carcinogenesis , cancer research , biology , catenin , microbiology and biotechnology , apoptosis , cancer , genetics , gene , signal transduction , biochemistry , protease , peptide hydrolases , enzyme
CSN5/JAB1 is a critical subunit of the COP9 signalosome (CSN) and is overexpressed in many human cancers, but little is known about the role of CSN5 in colorectal cancer (CRC). To explore the functional role of CSN5 in colorectal tumorigenesis, we applied siRNA technology to silence CSN5 in HeLa, SW480, HCT116, HT29, and CaCo2 cells. CSN5 knock‐down led to reduced β‐catenin and phospho‐β‐catenin levels and this was paralleled by reduced CRC cell proliferation and reduced apoptosis rates, whereas the short‐term β‐catenin protein stability was enhanced by CSN5 knock‐down in SW480 cells. Together, these data implicate the CSN in the pathogenesis of CRC via regulation of the Wnt/β‐catenin pathway.