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題名 | Etoposide (VP-16)誘導p53缺失非小細胞肺癌細胞的凋亡=Etoposide (VP-16)-induced Apoptosis in Human Non-small Cell Lung Cancer Cells Lacking Endogenous p53 |
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作者 | 邱建智; 李慶孝; 吳文慧; 傅子憲; 陳韋倫; 方剛; Chiu, Chien-chih; Li, Ching-hsiao; Ung, Man-wai; Fu, Tzu-hsieh; Chen, Wei-lun; Fang, Kang; |
期刊 | BioFormosa |
出版日期 | 20040600 |
卷期 | 39:1 2004.06[民93.06] |
頁次 | 頁15-22 |
分類號 | 418.2216 |
語文 | chi |
關鍵詞 | 細胞凋亡; 人類非小細胞肺癌; VP-16; Etoposide; Caspase-7; Caspase-9; Human non-small cell lung cancer; Apoptosis; |
中文摘要 | VP-16是一種廣泛被使用的抗癌藥劑,其主要的作用機制是抑制topoisomerase IIα的活性,阻斷DNA的複製,造成腫瘤細胞生長停滯甚至死亡,以達到消滅腫瘤的目的。本研究發現低劑量(5 µM) VP-16可以誘導p53基因缺失的非小細胞肺癌細胞株(NSCLC) H1299的細胞凋亡(apoptosis)。實驗證明VP-16誘導H1299在凋亡的過程中,caspase酵素群扮演相當重要的角色,進一步的分析也發現caspase的活化與凋亡的過程密切關聯(caspase-dependent)。綜合而論,低劑量VP-16誘導p53基因缺失H1299細胞的凋亡模式中,caspase-9可能參與細胞凋亡早期誘導作用,而caspase-7則與凋亡晚期的DNA片段化(fragmentation)有關,試驗中並得知caspase-7抑制劑無法阻止細胞凋亡,推論VP-6除了誘導caspase活化所引起細胞凋亡,同時也活化其他因子參與凋亡的過程。 |
英文摘要 | VP-16 (etoposide), an inhibitor of topoisomerase IIα, was widely used for cancer therapy. We found low dosage of VP-16 causes apoptosis in cancer cells without functional p53. In this work, we have identified that caspases were responsible for the progression of apoptosis in VP-16-induced H1299 cells lacking endogenous p53. Further study showed that apoptosis effectors caspase-9 and caspase-7 were activated prior to apoptosis. This work also demonstrated that VP-16-induced apoptosis in human non-small cell lung cancer cells is independent of p53 status. |
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