肿瘤研究与临床
腫瘤研究與臨床
종류연구여림상
CANCER RESEARCH AND CLINIC
2010年
8期
543-546
,共4页
戴亚丽%叶静%姜志茹%彭卫群%林远%蓝薇
戴亞麗%葉靜%薑誌茹%彭衛群%林遠%藍薇
대아려%협정%강지여%팽위군%림원%람미
甲状腺肿瘤%甲基化%受体,促甲状腺素%基因,p16%启动区(遗传子)
甲狀腺腫瘤%甲基化%受體,促甲狀腺素%基因,p16%啟動區(遺傳子)
갑상선종류%갑기화%수체,촉갑상선소%기인,p16%계동구(유전자)
Thyroid neoplasms%Methylation%Receptors,thyrotropin%Genes,p16%Promoter regions (genetics)
目的 研究促甲状腺激素受体(TSHR)和p16抑癌基因在甲状腺乳头状癌的表达及启动子甲基化的情况,分析两种抑癌基因的甲基化状况与肿瘤发生的关系.方法 对50例甲状腺乳头状癌组织和32例对照组织(20例结节性甲状腺肿,12例甲状腺腺瘤)提取RNA后,反转录为cDNA,进行PCR,检测两种抑癌基因mBNA的表达情况,运用甲基化PER(其中p16使用巢氏甲基化PCR)检测上述组织中两种抑癌基因启动子区甲基化的情况,对两种抑癌基因甲基化和未甲基化的组织随机进行测序.结果 甲状腺乳头状癌组50例患者中,有34例(68%)TSHR基因、27例(54%)的p16基因启动子发生了甲基化;对照组32例患者中,有7例(21.9%)TSHR基因、5例(15.6%)的p16基因启动子发生了甲基化;甲状腺乳头状癌组TSHB基因、p16基凶启动子甲基化率均显著高于对照组,差异有统计学意义(χ2=16.61,P<0.05;χ2=12.08,P<0.05).TSHR基因和p16基因mRNA在甲状腺乳头状癌中的表达量分别为0.41±0.11、0.51±0.17,相应的对照组织的mRNA的表达量分别为0.63±0.08、0.72±0.22,两种基因的mRNA在甲状腺乳头状癌中的表达明显低于对照组织,差异有统计学意义(t值分别为3.86和3.66,P<0.05).最终,经DNA测序证实,两种抑癌基因启动子发生甲基化的其CpG岛的碱基未发生改变,仍为CG;未发生甲基化的,碱基由CG变为TG.结论 两种抑癌基因启动子甲基化与甲状腺乳头状癌的发生和发展均相关.
目的 研究促甲狀腺激素受體(TSHR)和p16抑癌基因在甲狀腺乳頭狀癌的錶達及啟動子甲基化的情況,分析兩種抑癌基因的甲基化狀況與腫瘤髮生的關繫.方法 對50例甲狀腺乳頭狀癌組織和32例對照組織(20例結節性甲狀腺腫,12例甲狀腺腺瘤)提取RNA後,反轉錄為cDNA,進行PCR,檢測兩種抑癌基因mBNA的錶達情況,運用甲基化PER(其中p16使用巢氏甲基化PCR)檢測上述組織中兩種抑癌基因啟動子區甲基化的情況,對兩種抑癌基因甲基化和未甲基化的組織隨機進行測序.結果 甲狀腺乳頭狀癌組50例患者中,有34例(68%)TSHR基因、27例(54%)的p16基因啟動子髮生瞭甲基化;對照組32例患者中,有7例(21.9%)TSHR基因、5例(15.6%)的p16基因啟動子髮生瞭甲基化;甲狀腺乳頭狀癌組TSHB基因、p16基兇啟動子甲基化率均顯著高于對照組,差異有統計學意義(χ2=16.61,P<0.05;χ2=12.08,P<0.05).TSHR基因和p16基因mRNA在甲狀腺乳頭狀癌中的錶達量分彆為0.41±0.11、0.51±0.17,相應的對照組織的mRNA的錶達量分彆為0.63±0.08、0.72±0.22,兩種基因的mRNA在甲狀腺乳頭狀癌中的錶達明顯低于對照組織,差異有統計學意義(t值分彆為3.86和3.66,P<0.05).最終,經DNA測序證實,兩種抑癌基因啟動子髮生甲基化的其CpG島的堿基未髮生改變,仍為CG;未髮生甲基化的,堿基由CG變為TG.結論 兩種抑癌基因啟動子甲基化與甲狀腺乳頭狀癌的髮生和髮展均相關.
목적 연구촉갑상선격소수체(TSHR)화p16억암기인재갑상선유두상암적표체급계동자갑기화적정황,분석량충억암기인적갑기화상황여종류발생적관계.방법 대50례갑상선유두상암조직화32례대조조직(20례결절성갑상선종,12례갑상선선류)제취RNA후,반전록위cDNA,진행PCR,검측량충억암기인mBNA적표체정황,운용갑기화PER(기중p16사용소씨갑기화PCR)검측상술조직중량충억암기인계동자구갑기화적정황,대량충억암기인갑기화화미갑기화적조직수궤진행측서.결과 갑상선유두상암조50례환자중,유34례(68%)TSHR기인、27례(54%)적p16기인계동자발생료갑기화;대조조32례환자중,유7례(21.9%)TSHR기인、5례(15.6%)적p16기인계동자발생료갑기화;갑상선유두상암조TSHB기인、p16기흉계동자갑기화솔균현저고우대조조,차이유통계학의의(χ2=16.61,P<0.05;χ2=12.08,P<0.05).TSHR기인화p16기인mRNA재갑상선유두상암중적표체량분별위0.41±0.11、0.51±0.17,상응적대조조직적mRNA적표체량분별위0.63±0.08、0.72±0.22,량충기인적mRNA재갑상선유두상암중적표체명현저우대조조직,차이유통계학의의(t치분별위3.86화3.66,P<0.05).최종,경DNA측서증실,량충억암기인계동자발생갑기화적기CpG도적감기미발생개변,잉위CG;미발생갑기화적,감기유CG변위TG.결론 량충억암기인계동자갑기화여갑상선유두상암적발생화발전균상관.
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.
