A study on the promoter hypermethylation of TSHR and pl6 gene in human papillary thyroid carcinoma
10.3760/cma.j.issn.1006-9801.2010.08.013
- VernacularTitle:抑癌基因促甲状腺激素受体和p16启动子甲基化与甲状腺乳头状癌关系的研究
- Author:
Yali DAI
;
Jing YE
;
Zhiru JIANG
;
Weiqun PENG
;
Yuan LIN
;
Wei LAN
- Publication Type:Journal Article
- Keywords:
Thyroid neoplasms;
Methylation;
Receptors,thyrotropin;
Genes,p16;
Promoter regions (genetics)
- From:
Cancer Research and Clinic
2010;22(8):543-546
- CountryChina
- Language:Chinese
-
Abstract:
Objective To study the expression of the tumor suppressor gene TSHR and pl6 in papillary thyroid carcinoma (PTC) and explore the relationship of the tumorigenesis and the promoter aberrant methylation of the two above genes. Methods RT-PCR was used to detect the mRNA expression of two tumor suppressor genes in 50 cases of PTC, 20 cases of nodular goiter and 12 cases of thyroid adenoma tissue. The promoter methylation status of the two genes were detected by methylation-specific PCR technique (MSP) (which of p16 by nested PCR). The promoter hypermethylation of the two genes was tested by randomly gene sequencing. Results Hypermethylation of promoter region were detected from 68.0 % (34/50) TSHR gene and 54.0 % (27/50) pl6 gene in PTC, while 21.9 % (7/32) and 15.60 % (5/32) in controls. The rate of promoter methylation in PTC was significantly higher than that in controls (χ2 = 16.61, P <0.05 vs χ2 =12.08 P <0.05). The relative mRNA expression of TSHR gene and pl6 gene were (0.41±0.11) and (0.51±0.17) in PTC, respectively, while those were (0.63 ±0.08) and (0.72 ±0.22) in controls, respectively. The mRNA expression of the TSHR gene and pl6 gene was obviously lower in PTC than that in controls (t = 3.86, P < 0.05 vs t =3.66, P <0.05). By the sequencing, it was confirmed that the CG in methylated promoter of the two genes was not changed, while the CG in unmethylated promoter was changed into TG. Conclusion Methylation of the TSHR gene and p16 gene in promoter region is a common molecule event and may be invovled in the genesis and development of human PTC.
