高表达bcl-2卵巢癌细胞系参与药物抵抗和细胞凋亡作用的研究  

The Control of Apoptosis and Drug Resistance in Ovarian Cancer Cells Which Overexpressed bcl-2

作　　者：田方[1] 李春海[1] 颜春洪[1] 陈高明[1] 

机构地区：[1]军事医学科学院附属医院肿瘤分子生物室,北京100850

出　　处：《中国肿瘤生物治疗杂志》2000年第2期106-108,共3页Chinese Journal of Cancer Biotherapy

基　　金：中国博士后基金!(98623);自然科学基金!(39870784)共同资助

摘　　要：目的：探讨化疗的敏感性与细胞凋亡的关系，观察细胞凋亡抑制分子ｂｃｌ－２在卵巢癌化疗抵抗中的作用。方法：构建了逆转录病毒ｂｃｌ－２表达载体ｐＬＸＳＮ／ｂｃｌ－２，应用ｌｉｐｏｆａｃｔｉｎ法建立转染ｂｃｌ－２基因和转染空载体ｐＬＸＳＮ的卵巢癌细胞系。ＭＴＴ法观察细胞系抵抗药物的细胞毒作用。ＦＡＣＳ和ＤＮＡ琼脂糖凝胶电泳观察ｂｃｌ－２高表达细胞系在阿霉素诱导细胞凋亡中的变化。结果：转染 ｂｃｌ－２的卵巢癌细胞系ＯＣ３／ｂｃｌ－２稳定表达ｂｃｌ－２分子并抵抗药物介导的细胞毒作用，明显提高细胞的存活率，与此同时也抑制细胞凋亡的发生。结论：化疗的敏感性与细胞凋亡的调节密切相关，凋亡抑制基因ｂｃｌ－２在肿瘤耐药中起重要作用。Objective: To investigate whether bcl-2 directly contributes to the development of drug resistance and apoptosis in o- varian cancer cell lines cells OC3. Methods: Retrovirus expression cector pLXSN-bcl-2 was constructed and was transfected to ovarian cancer cell line cells OC3 using Lipofectin,with empty vector pLXSN as a control. bcl-2 expession of transfected cells was analyzed by FACS and Western blot and Adr-induced cytotoxicity was measured by MTT assay. Apoptosis was also detected by PI DNA staining and DNA Ladder analysis.Results:pLXSN/bcl-2 transfected cells OC3/bcl-2 overexpressed bcl-2 and were resistant to Adr-induced cytotoxicity.The ability against Adr-induced apoptosis was increased. Conclusion: bcl-2 may play an important role in the resistance to Adr-inducing apoptosis, thereby increasing resistance of OC3/bcl-2 cells to chemotherapy.

关 键 词：BCL-2 药物抵抗 细胞凋亡 卵巢肿瘤 

分 类 号：R737.31[医药卫生—肿瘤]