生物技术通报
生物技術通報
생물기술통보
BIOTECHNOLOGY BULLETIN
2010年
2期
140-144
,共5页
潘翠翠%罗春丽%吴小候%杨淑哲%荀春华%蒲军
潘翠翠%囉春麗%吳小候%楊淑哲%荀春華%蒲軍
반취취%라춘려%오소후%양숙철%순춘화%포군
肾癌%hepeCAM%甲基化
腎癌%hepeCAM%甲基化
신암%hepeCAM%갑기화
Renal carcinoma%HepaCAM%Methylation
探讨肾癌中抑癌基因肝细胞粘附分子hepaCAM表达与hepaCAM外显子2 CpG岛甲基化状态的关系.采用甲基化敏感性限制性内切酶PCR、RT-PCR法检测肾癌细胞株(786-0,RC-2)和43例肾癌及相应的癌旁组织中hepaCAM外显子2的甲基化状态及hepaCAM mRNA的表达.786-0细胞hepaCAM表达水平低于RC-2细胞(P＜0.05);786.0和RC-2细胞,前者存在hepaCAM外显子2甲基化,后者未检测到.肾癌组织中hepaCAM mRNA表达水平显著低于癌旁组织(P＜0.001);肾癌组织hepaCAM外显子2的甲基化率为34.9%,癌旁组织2.33%,两者差异有显著意义(P＜0.001),但在临床病理参数中的差异无统计学意义(P＞0.05).hepaCAM外显子2甲基化的肾癌组织其mRNA的表达水平显著低于未甲基化的肾癌组织(P＜0.05).因此,肾癌hepaCAM外显子2的甲基化可能是导致hepaCAM表达下降或缺失的原因之一,hepaCAM甲基化的研究为探讨肾癌发生发展的机制提供了新的理论依据.
探討腎癌中抑癌基因肝細胞粘附分子hepaCAM錶達與hepaCAM外顯子2 CpG島甲基化狀態的關繫.採用甲基化敏感性限製性內切酶PCR、RT-PCR法檢測腎癌細胞株(786-0,RC-2)和43例腎癌及相應的癌徬組織中hepaCAM外顯子2的甲基化狀態及hepaCAM mRNA的錶達.786-0細胞hepaCAM錶達水平低于RC-2細胞(P＜0.05);786.0和RC-2細胞,前者存在hepaCAM外顯子2甲基化,後者未檢測到.腎癌組織中hepaCAM mRNA錶達水平顯著低于癌徬組織(P＜0.001);腎癌組織hepaCAM外顯子2的甲基化率為34.9%,癌徬組織2.33%,兩者差異有顯著意義(P＜0.001),但在臨床病理參數中的差異無統計學意義(P＞0.05).hepaCAM外顯子2甲基化的腎癌組織其mRNA的錶達水平顯著低于未甲基化的腎癌組織(P＜0.05).因此,腎癌hepaCAM外顯子2的甲基化可能是導緻hepaCAM錶達下降或缺失的原因之一,hepaCAM甲基化的研究為探討腎癌髮生髮展的機製提供瞭新的理論依據.
탐토신암중억암기인간세포점부분자hepaCAM표체여hepaCAM외현자2 CpG도갑기화상태적관계.채용갑기화민감성한제성내절매PCR、RT-PCR법검측신암세포주(786-0,RC-2)화43례신암급상응적암방조직중hepaCAM외현자2적갑기화상태급hepaCAM mRNA적표체.786-0세포hepaCAM표체수평저우RC-2세포(P＜0.05);786.0화RC-2세포,전자존재hepaCAM외현자2갑기화,후자미검측도.신암조직중hepaCAM mRNA표체수평현저저우암방조직(P＜0.001);신암조직hepaCAM외현자2적갑기화솔위34.9%,암방조직2.33%,량자차이유현저의의(P＜0.001),단재림상병리삼수중적차이무통계학의의(P＞0.05).hepaCAM외현자2갑기화적신암조직기mRNA적표체수평현저저우미갑기화적신암조직(P＜0.05).인차,신암hepaCAM외현자2적갑기화가능시도치hepaCAM표체하강혹결실적원인지일,hepaCAM갑기화적연구위탐토신암발생발전적궤제제공료신적이론의거.
It was to investigate the relationship between the expression of hepaCAM and methylation of hepaCAM exon 2 in renal carcinoma.Methylation-specific restriction-PCR-assay and reverse transcription-polymerse chain reaction(RT-PCR)were used to examine the methylation status of hepaCAM exon 2 and mRNA in renal carcinoma cell lines(786-0,RC-2)and 43 cases of renal carcinoma tissues and paired adjacent tissues.The expression of hepaCAM mRNA was down-regulated in 786-0 renal cell lines as compared with RC-2 renal cell lines(P＜0.05);786-0 cell lines showed hepaCAM exon 2 methylation but RC-2 didn't.The expression of hepaCAM mRNA in renal carcinomas was significant lower than that in the adjacent renal tissues(P＜0.001).The methylation rate of hepaCAM exon 2 was significant higher in renal carcinomas than in adjacent renal tissues(34.9%vs2.33%,P＜0.001).But,there was no statistically significant difference in clinical pathology parameters(P＞0.05).The expression of hepaCAM mRNA was significant lower in hepaCAM exon 2 methylation renal carcinoma than that in unmethylated renal carcinoma(P＜0.05).Therefore,the methylation of hepaCAM exon 2 seems to be one of reasons inducing the down-regulation or deletion of hepaCAM expression.The study of hepaCAM methylation provides a new theoretical evidence for the mechanism of the occurrence and development of renal carcinoma.
