摘要:目的探讨人乳腺癌AKT通路与乳腺癌TG2调节EPI耐药性关系。方法构建TGM2基因慢病毒过表达载体(TGM2-LV),转染MCF-7细胞,设TG2组、Nc组和MK2206组。MCF-7/adr细胞,设ADR组和MKadr组。westernBlot检测乳腺癌细胞TG2、AKT、Bcl-2和P53表达。EPI加入各组细胞中,MTT法检测细胞增殖作用,TUNEL法对EPI诱导肿瘤细胞凋亡检测。结果TG2组相对NC组TG2、Bcl-2和p-AKT表达明显升高,P53表达下降(P〈0.05)。MK2206组(MKadr组)相较TG2组(ADR组),Bcl-2表达和p-AKT活性下降,P53表达上升。EPI作用后,TG2组相对Nc组增殖作用增强。MK2206组(MKadr组)相较TG2组(ADR组)抑制细胞增殖作用。MK2206组(MKadr组)细胞凋亡率高于TG2组(ADR组)(P〈0.05)。结论TG2表达可能通过AKT通路调节乳腺癌细胞EPI耐药性。
注:因版权方要求,不能公开全文,如需全文,请咨询杂志社
热门期刊服务
Control Theory and Technology Journal of Energy Chemistry Current Zoology High Technology Letters China Petroleum Processing Petrochemical Technology Tsinghua Science and Technology Journal of Integrative Plant Biology World Journal of Gastroenterology Journal of Wuhan University of Technology Journal of Tropical Meteorology Journal of Huazhong University of Science and Technology Frontiers of Information Technology Electronic Engineering