Document Detail


HEF1 is a crucial mediator of the proliferative effects of prostaglandin E(2) on colon cancer cells.
MedLine Citation:
PMID:  20068165     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Prostaglandin E(2) (PGE(2)), one of the downstream products of cyclooxygenase-2 enzymatic activity, promotes colorectal carcinogenesis in part by stimulating cell division. In this study, we define a critical mechanism in this process by showing that the prometastatic adapter protein human enhancer of filamentation 1 (HEF1; NEDD9) links PGE(2) to the cell cycle machinery in colorectal cancer cells. PGE(2) rapidly induced expression of HEF1 mRNA and protein in colorectal cancer cells. HEF1 overexpression elicited the same effects as PGE(2) treatment on cell proliferation, cell cycle progression, and tumor growth. Conversely, HEF1 knockdown suppressed PGE(2)-driven cell proliferation and cell cycle progression. Cell cycle alterations involved HEF1 fragmentation as well as co-distribution of HEF1 and cell cycle kinase Aurora A along spindle asters during cell division. Moreover, Aurora A co-immunoprecipitated with HEF1 and was activated by HEF1. Consistent with a role for HEF1 in colorectal carcinogenesis, we found elevated expression of HEF1 expression in 50% of human colorectal cancers examined, relative to paired normal tissues. These findings establish that PGE(2) induces HEF1 expression, which in turn promotes cell cycle progression through its interaction with and activation of Aurora A. Further, they establish that HEF1 is a crucial downstream mediator of PGE(2) action during colorectal carcinogenesis.
Authors:
Dianren Xia; Vijaykumar R Holla; Dingzhi Wang; David G Menter; Raymond N DuBois
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2010-01-12
Journal Detail:
Title:  Cancer research     Volume:  70     ISSN:  1538-7445     ISO Abbreviation:  Cancer Res.     Publication Date:  2010 Jan 
Date Detail:
Created Date:  2010-01-15     Completed Date:  2010-03-09     Revised Date:  2011-07-19    
Medline Journal Info:
Nlm Unique ID:  2984705R     Medline TA:  Cancer Res     Country:  United States    
Other Details:
Languages:  eng     Pagination:  824-31     Citation Subset:  IM    
Affiliation:
Department of Cancer Biology, The University of Texas M.D. Anderson Cancer Center, Houston, Texas 77030, USA.
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MeSH Terms
Descriptor/Qualifier:
Adaptor Proteins, Signal Transducing / biosynthesis*,  genetics
Animals
Cell Cycle / drug effects
Cell Growth Processes / drug effects
Cell Line, Tumor
Colorectal Neoplasms / genetics,  metabolism*,  pathology*
Dinoprostone / pharmacology*
Humans
Mice
Mice, Nude
Phosphoproteins / biosynthesis*,  genetics
Protein-Serine-Threonine Kinases / metabolism
RNA, Messenger / biosynthesis,  genetics
Grant Support
ID/Acronym/Agency:
P01 CA077839-10/CA/NCI NIH HHS; P01 CA77839/CA/NCI NIH HHS; R01 DK062112-09/DK/NIDDK NIH HHS; R25T CA57730/CA/NCI NIH HHS; R37 DK047297-16/DK/NIDDK NIH HHS; R37 DK047297-18/DK/NIDDK NIH HHS; R37 DK47297/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Adaptor Proteins, Signal Transducing; 0/NEDD9 protein, human; 0/Phosphoproteins; 0/RNA, Messenger; 363-24-6/Dinoprostone; EC 2.7.11.1/Protein-Serine-Threonine Kinases; EC 2.7.11.1/aurora kinase
Comments/Corrections

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