Study on the promoter hypermethylation of TSHR, P16, and RAS genes in human papillary thyroid carcinoma
10.3760/cma.j.issn.1000-6699.2010.05.010
- VernacularTitle:乳头状甲状腺癌抑癌基因TSHR、P16和RAS启动子甲基化研究
- Author:
Yali DAI
;
Jing YE
;
Fan ZHANG
;
Yuan LIN
;
Weiqun PENG
;
Donghui LU
;
Lingchuan HAN
- Publication Type:Journal Article
- Keywords:
Papillary thyroid carcinoma;
Methylation;
TSHR;
P16;
RAS;
Promoter
- From:
Chinese Journal of Endocrinology and Metabolism
2010;26(5):381-384
- CountryChina
- Language:Chinese
-
Abstract:
Objective To study the expressions of the tumor suppressor gene TSH receptor( TSHR),P16, and RAS in papillary thyroid carcinoma ( PTC ) , and the correlation between the occurrence of tumor and the aberrant promoter hypermethylation of three tumor suppressor genes. Methods RT-PCR was used to detect the mRNA expression of three tumor suppressor genes in tissues of 50 cases of PTC ,20 cases of nodular goiter,and 12 cases of thyroid adenoma. The promoter methylation status of three tumor suppressor genes was examined by methylation-specific PCR technique( MSP). Gene sequencing was used to test if the hypermethylation existed in the promoter of three tumor suppressor genes. Results In 68.0% (34/50) TSHR gene, 54.0% (27/50) P16 gene, and 60.0% ( 30/50 ) RAS gene in PTCs, hypermethylation in promoter region was detected, the respective results 21.9% (7/32) , 15. 6% (5/32) ,and 31. 3% (10/32) were found in control tissues. The rates of the three genes with promoter hypermethylation in PTC were significantly higher than those in control tissues ( all P<0. 05). The mRNA expressions of TSHR,P16,and RAS were significantly lower in PTC than those in control tissues (0. 41 ± 0.11 vs 0.63±0. 08,0. 51±0. 17 vs 0. 72±0. 22,0. 56±0. 10 vs 0. 67±0. 16, all P<0. 05). The sequencing confirmed that there was CC to TC transmission in the promoters of three tumor suppressor genes. Conclusions The methylation of three tumor suppressor genes in promoter region is a common molecule event and may be involved in the genesis and development of human PTC.