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Galectin-3 stabilizes heterogeneous nuclear ribonucleoprotein Q to maintain proliferation of human colon cancer cells
Authors:B. C. Yoo  S-H. Hong  J-L. Ku  Y-H. Kim  Y-K. Shin  S-G. Jang  I-J. Kim  S-Y. Jeong  J-G. Park
Affiliation:(1) Research Institute, National Cancer Center, Madu2-dong, Goyang-si, 410–769, Gyeonggi-do, Korea;(2) Cancer Research Institute and Cancer Research Center, Seoul National University, Yeongeon-dong, Jongno-gu, Seoul, 110–744, Korea;(3) UCSF Comprehensive Cancer Center, University of California, San Francisco, CA 94143, USA
Abstract:Comparative analysis of proteomes using 5-fluorouracil (5-FU)-resistant human colon cancer cell line revealed that decreased galectin-3 expression was significantly associated with retarded proliferation. However, in the presence of 5-FU proliferation rate of cells with suppressed galectin-3 expression did not differ from that of cells with normal galectin-3 expression, even galectin-3 suppression augmented apoptosis. Mechanism by which galectin-3 regulates cancer cell proliferation has been identified in immunoprecipitates of the anti-galectin-3 antibody. Heterogeneous nuclear ribonucleoprotein Q (hnRNP Q) was identified as a protein interacting with galectin-3. Interestingly, while galectin-3 protein was not affected by the hnRNP Q level, its suppression was accompanied by a decrease in hnRNP Q expression. The present study demonstrates that galectin-3 stabilizes hnRNP Q via complex formation, and reduction in the hnRNP Q level leads to slow proliferation and less susceptibility to 5-FU. Electronic supplementary material  The online version of this article (doi:) contains supplementary material, which is available to authorized users. B.C.Yoo; S-H.Hong; These two authors contributed equally to this work. Received 10 September 2008; received after revision 19 October 2008; accepted 07 November 2008
Keywords:  KeywordHeading"  >. Galectin-3  hnRNP Q  colon cancer  proliferation  protein stability  5-fluorouracil
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