Transient and etiology-related transcription regulation in cirrhosis prior to hepatocellular carcinoma occurrence.
World J Gastroenterol, 2009/1/21;15(3):300-9.
Caillot F[1], Derambure C, Bioulac-Sage P, Francois A, Scotte M, Goria O, Hiron M, Daveau M, Salier JP
Affiliations
PMID: 19140229
Impact factor: 5.374
Abstract
aim: To search for transcription dysregulation that could (1) differentiate hepatocellular carcinoma (HCC)-free from HCC-related cirrhosis (2) differentiate HCC-free cirrhosis related to HCV from that related to alcohol intake.
methods: Using microarray analysis, we compared transcript levels in HCC-free cirrhosis (alcoholism: 7; hepatitis C: 7), HCC-associated cirrhosis (alcoholism: 10; hepatitis C: 10) and eight control livers. The identified transcripts were validated by qRT-PCR in an independent cohort of 45 samples (20 HCC-free cirrhosis; 15 HCC-associated cirrhosis and 10 control livers). We also confirmed our results by immunohistochemistry.
results: In HCC-free livers, we identified 70 transcripts which differentiated between alcoholic-related cirrhosis, HCV-related cirrhosis and control livers. They mainly corresponded to down-regulation. Dysregulation of Signal Transduction and Activator of Transcription-3 (STAT-3) was found along with related changes in STAT-3 targets which occurred in an etiology-dependent fashion in HCC-free cirrhosis. In contrast, in HCC, such transcription dysregulations were not observed.
conclusion: We report that transcriptional dysregulations exist in HCC-free cirrhosis, are transiently observed prior to detectable HCC onset and may be appear like markers from cirrhosis to HCC transition.
MeSH terms
Adult; Aged; Carcinoma, Hepatocellular; Female; Gene Expression Profiling; Gene Expression Regulation, Neoplastic; Gene Regulatory Networks; Humans; Liver Cirrhosis; Liver Neoplasms; Male; Middle Aged; Oligonucleotide Array Sequence Analysis; Plasminogen; Transcription, Genetic
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