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作 者:龙胜文 尹梓豪 许斐钰 丁小凤[1] LONG Shengwen;YIN Zihao;XU Feiyu;DING Xiaofeng(Key Laboratory of Developmental Biology of Freshwater Fish,College of Life Science,Hunan Normal University,Changsha 410081,China)
机构地区:[1]湖南师范大学生命科学学院淡水鱼类发育生物学国家重点实验室
出 处:《激光生物学报》2020年第1期54-60,74,共8页Acta Laser Biology Sinica
基 金:国家自然科学基金项目(81770389,81872256)
摘 要:为了深入探讨乳腺癌治疗耐药的发生机制并寻找乳腺癌治疗耐药的潜在治疗手段,我们以乳腺癌MCF-7和耐阿霉素MCF-7/ADR细胞为研究对象,研究RNA甲基化酶WTAP对其迁移的影响。MTT试验发现阿霉素对MCF-7细胞活力的抑制作用大于对MCF-7/ADR细胞的抑制作用。qPCR和western-blot试验发现WTAP在耐阿霉素细胞MCF-7/ADR中高表达,同时transwell试验发现在MCF-7细胞中增加WTAP的表达对MCF-7细胞的迁移没有影响,而在MCF-7/ADR细胞中敲低WTAP的表达会抑制MCF-7/ADR细胞的迁移。western-blot试验进一步证明了这一作用是通过抑制上皮间质转化(EMT)来发挥的。这一发现有助于为乳腺癌的临床治疗提供新的理论依据并为乳腺癌的治疗提供新的策略。To investigate the molecular mechanisms of breast cancer resistance progression and develop novel potential therapeutic methods for the treatment of breast cancer resistance,in the study,the role of wtap in the cell migration of breast cancer MCF-7 and adriamycin resistant MCF-7/ADR cells were determined.MTT assays showed that adriamycin inhibited the survival of MCF-7 cells more than MCF-7/ADR did.qPCR and western-blot assays showed that WTAP was highly expressed in adriamycin resistant MCF-7/ADR cells.Moreover,transwell assays showed that increasing WTAP expression in MCF-7 cells had no effect on the migration of MCF-7 cells,whereas knocking down WTAP expression in MCF-7/ADR cells can inhibit the migration of MCF-7/ADR cells,which may be affected by inhibiting epithelial-mesenchymal transition(EMT)detected by western-blot.This finding will provide a new theoretical basis and strategy for the clinical treatment of breast cancer.
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