粒線體DNA突變在大腸癌病患正常結腸與癌化組織之比較

人類正常細胞在複製完成有限的細胞週期(cell cycle)複製之後或是遭受到嚴重的損傷，會引發細胞凋亡(Apoptosis)，而癌化的細胞並沒有此現象，甚至於促進細胞走向永生(immortal)。雖然細胞的永生(immortal)另與端粒酶(telemerase)有相當的關係，但是更有研究指出，在癌症的組織細胞中，粒線體DNA(mtDNA)的拷貝數量(copy number)會與正常的組織不同，然而在正常的組織細胞中粒線體在參與調控細胞凋亡的過程中扮演非常重要角色。故本篇研究實驗乃是觀察在大腸直腸癌患者之正常組織與癌細胞之粒線體DNA是否發生突變，本篇實驗針對60位大腸癌症病患，研究對於細胞走向老化現象相關的粒線體DNA 4977bp deletion (common deletion )的發生情形。結果顯示每一個體之非癌化的大腸組織中可以偵測出其粒線體DNA具有deletion的突變，而癌細胞的粒線體DNA則無偵測出deletion的現象。這結果可能代表著粒線體DNA在癌化細胞中比正常細胞較不走向老化，或者顯示因為癌化細胞的快速分裂，而使得具有 deletion的粒線體DNA被稀釋所致｡

Limited replication or injury may induce apoptosis in normal human cells, but not in cancer cells .Telemerase activity may be another contributor to immortality of cancer cells .Recently, it was found that the copy numbers of mitochondrial DNA(mtDNA) in cancer cells are different from that of corresponding non-cancer cells .This observation suggest that mitochondrial DNA plays an important role in the carcinogenesis of human cancer.In this thesis ,it was analyzed that mtDNA mutation occurs in the colon cancer and corresponding non-cancer colon tissue .The result showed that the common deletion in mtDNA was detected in non-cancer colon tissue but not in the colon cancer.This result suggest that mt DNA mutation may play an important role in the carcinogenesis of colon cancer and the mtDNA with deletion may be diluted by rapid cell division in colon cancers.