Methylation of RAR-β2, RASSF1A, and CDKN2A genes induced by nickel subsulfide and nickel-carcinogenesis in rats.
- Author:
Jun ZHANG
1
;
Jing ZHANG
;
MengJie LI
;
YouJun WU
;
YingYing FAN
;
Yang ZHOU
;
LiLi TAN
;
ZhiHua SHAO
;
HongJun SHI
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Carcinogens; toxicity; CpG Islands; Cyclin-Dependent Kinase Inhibitor p16; genetics; metabolism; DNA Methylation; Gene Expression Regulation, Neoplastic; drug effects; Lung Neoplasms; chemically induced; metabolism; Male; Muscle Neoplasms; chemically induced; metabolism; Nickel; toxicity; Rats; Rats, Wistar; Receptors, Retinoic Acid; genetics; metabolism; Tumor Suppressor Proteins; genetics; metabolism
- From: Biomedical and Environmental Sciences 2011;24(2):163-171
- CountryChina
- Language:English
-
Abstract:
OBJECTIVETo investigate the expression variation of RAR-β2, RASSF1A, and CDKN2A gene in the process of nickel-induced carcinogenesis.
METHODSNickel subsulfide (Ni(3)S(2)) at dose of 10 mg was given to Wistar rats by intramuscular injection. The mRNA expression of the three genes in induced tumors and their lung metastasis were examined by Real-time PCR. The methylation status of the 5' region of these genes were detected by Quantitative Real-time methylation specific PCR.
RESULTSThe mRNA expressions of the three genes both in muscle and lung tumor were decreased distinctly in comparison with normal tissue. But hypermethylation was found only in muscle tumor.
CONCLUSIONThese findings suggest that loss of function or decrease of RAR-β2, RASSF1A, and CDKN2A, as well as the hypermethylation of 5' region of these genes, are related with nickel exposure.
