PMID- 19666411
OWN - NLM
STAT- MEDLINE
DCOM- 20100119
LR  - 20131121
IS  - 1499-3872 (Print)
VI  - 8
IP  - 4
DP  - 2009 Aug
TI  - Quantitative analysis of hepatic hypoxia-inducible factor-1alpha and its abnormal 
      gene expression during the formation of hepatocellular carcinoma.
PG  - 407-13
AB  - BACKGROUND: Hepatic hypoxia-inducible factor-1 (HIF-1) is activated in the 
      progression of hepatocellular carcinoma (HCC). This study aimed to investigate 
      the dynamic alterations of HIF-1alpha and its gene expression so as to explore 
      the relationship between HIF-1alpha expression and hepatocarcinogenesis at the 
      early stage of HCC. METHODS: A hepatoma model was made with 2-fluorenyl-acetamide 
      (2-FAA) in male Sprague-Dawley rats. Morphological changes of rat hepatocytes 
      were assessed pathologically (HE staining). The dynamic expression of hepatic and 
      circulating HIF-1alpha was quantitatively analyzed by ELISA. The gene fragments 
      of hepatic HIF-1alpha mRNA were amplified by RT-PCR and confirmed by sequencing. 
      The cellular distribution of hepatic HIF-1alpha expression was confirmed by 
      immunohistochemistry. RESULTS: Histological examination confirmed granule-like 
      degeneration to atypical hyperplasia and HCC development in rat hepatocytes and 
      progressive increases in the levels of hepatic and circulating HIF-1alpha and its 
      gene expression during the course. The levels of HIF-1alpha expression in the 
      liver and blood of rats with hepatoma were significantly higher than those in 
      normal rats and those with degeneration. Immunohistochemical analysis confirmed 
      the positive expression and hepatocyte distribution of HIF-1alpha in the 
      development of rat hepatoma. A positive relationship was found between HIF-1alpha 
      expression in the liver and blood (P<0.01). CONCLUSIONS: The above observations 
      support the hypothesis that the overexpression of HIF-1alpha and its gene are 
      closely associated with the malignant transformation of hepatocytes and play an 
      important role at the stage of hepatocarcinogenesis.
FAU - Yao, Deng-Fu
AU  - Yao DF
AD  - Research Center of Clinical Molecular Biology, Affiliated Hospital of Nantong 
      University, Nantong 226001, China. yaodf@ahnmc.com
FAU - Jiang, Hua
AU  - Jiang H
FAU - Yao, Min
AU  - Yao M
FAU - Li, Yue-Ming
AU  - Li YM
FAU - Gu, Wen-Jing
AU  - Gu WJ
FAU - Shen, Yu-Cheng
AU  - Shen YC
FAU - Qiu, Li-Wei
AU  - Qiu LW
FAU - Wu, Wei
AU  - Wu W
FAU - Wu, Xin-Hua
AU  - Wu XH
FAU - Sai, Wen-Li
AU  - Sai WL
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Singapore
TA  - Hepatobiliary Pancreat Dis Int
JT  - Hepatobiliary & pancreatic diseases international : HBPD INT
JID - 101151457
RN  - 0 (Hif1a protein, rat)
RN  - 0 (Hypoxia-Inducible Factor 1, alpha Subunit)
RN  - 0 (RNA, Messenger)
RN  - 9M98QLJ2DL (2-Acetylaminofluorene)
SB  - IM
MH  - 2-Acetylaminofluorene
MH  - Animals
MH  - Base Sequence
MH  - Carcinoma, Hepatocellular/chemically induced/genetics/*metabolism/pathology
MH  - Cell Transformation, Neoplastic/chemically induced/genetics/*metabolism/pathology
MH  - Disease Models, Animal
MH  - Enzyme-Linked Immunosorbent Assay
MH  - *Gene Expression Regulation, Neoplastic
MH  - Hypoxia-Inducible Factor 1, alpha Subunit/blood/genetics/*metabolism
MH  - Immunohistochemistry
MH  - Liver/metabolism/pathology
MH  - Liver Neoplasms/chemically induced/genetics/*metabolism/pathology
MH  - Male
MH  - Molecular Sequence Data
MH  - Precancerous Conditions/chemically induced/genetics/*metabolism/pathology
MH  - RNA, Messenger/metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Up-Regulation
EDAT- 2009/08/12 09:00
MHDA- 2010/01/20 06:00
CRDT- 2009/08/12 09:00
PHST- 2009/08/12 09:00 [entrez]
PHST- 2009/08/12 09:00 [pubmed]
PHST- 2010/01/20 06:00 [medline]
AID - 1259 [pii]
PST - ppublish
SO  - Hepatobiliary Pancreat Dis Int. 2009 Aug;8(4):407-13.