Document Detail


Diabetes-associated angiotensin activation enhances liver metastasis of colon cancer.
MedLine Citation:
PMID:  22552372     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
We examined the effects of hyperglycemic conditions on liver metastasis of colorectal cancer (CRC). Angiotensin (A)-II increased growth, invasion, and anti-apoptotic survival in HT29 and CT26 cells. In contrast, angiotensinogen (ATG) increased these features in HT29 cells but not in CT26 cells. HT29 cells expressed A-II type 1 receptor, chymase, and rennin, whereas CT26 cells did not express renin. Renin expression and ATG-induced cell growth, invasion, and survival induced and increased as glucose concentration increased in HT29 cells and also CT26 cells. An inhibitor of renin or chymase abrogated A-II production in HT29 cells. Reduction of hepatic ATG production by cholesterol-conjugated antisense S-oligodeoxynucleotide suppressed liver metastasis of HT29 cells. An examination of 121 CRC patients showed that diabetes in CRC cases was associated with higher blood HbA1c, higher renin and A-II concentrations in the primary tumors, and higher incidence of liver metastasis than in nondiabetic cases. These results suggest that diabetes-associated angiotensin activation enhances liver metastasis of CRC and may therefore provide a possible target for antimetastatic therapy in CRC.
Authors:
Takasumi Shimomoto; Hitoshi Ohmori; Yi Luo; Yoshitomo Chihara; Ayumi Denda; Tomonori Sasahira; Naokuni Tatsumoto; Kiyomu Fujii; Hiroki Kuniyasu
Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2012-5-3
Journal Detail:
Title:  Clinical & experimental metastasis     Volume:  -     ISSN:  1573-7276     ISO Abbreviation:  -     Publication Date:  2012 May 
Date Detail:
Created Date:  2012-5-3     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8409970     Medline TA:  Clin Exp Metastasis     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Affiliation:
Department of Molecular Pathology, Nara Medical University, 840 Shijo-cho, Kashihara, Nara, 634-8521, Japan.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  hMLH1 promoter hypermethylation and MSI status in human endometrial carcinomas with and without meta...
Next Document:  Angiogenic factors in placentas from pregnancies complicated by fetal growth restriction (review).