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TG2通过AKT通路调节乳腺癌对表阿霉素耐药性 被引量:1

TG2 promotes drug resistance to epirubicin through AKT signal pathway in breast cancer
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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。Western Blot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。 Objective To investigate whether TG2 promotes drug resistance to epirubicin through AKT signal pathway in breast cancer. Methods MCF-7 cells with constant expression of TGM2 gene (TGM2-LV) were established via the lentiviral vector. The breast cancer cells were divided into five groups, including the NC group, TG2 group and MK2206 group. The MCF-7/adr cells were divided into ADR group and MKadr group. The expres- sion of TG2, AKT, Bcl-2 and P53 was detected by Western blot assay. Cells were treated with epirubicin. MTF assay was performed to assess cell proliferation. The inhibition ratio of cancer cell proliferation was evaluated. TUNEL analysis was performed to identify the apoptosis of the breast cancer cells. Results Lvels of TG2, p-AKT and Bcl-2 in NC group were significantly lower than those in TG2 group, while the expression of P53 in NC group was much higher. In MK2206 (or MK/adr ) group, p-AKT and Bcl-2 were down-regulated, while P53 was markedly up-regulated compared with TG2 (or ADR) group (P 〈 0.05 ). The results of the MTT assay showed a strong inhibi- tion in cell proliferation rate in MK2206 (or MKadr ) group. Compared with the NC group, TG2 promoted prolifera- tion of MCF-7 cells in TG2 group. The cell apoptosis rate in MK2206 (or MKadr ) group was significantly higher than that in TG2 (or ADR) group (P 〈 0.05). TG2 significantly inhibit the apoptosis of breast cancer cells, com- pared to the control group. Conclusion TG2 might promote drug resistance to epirubicin through AKT signal path- way in breast cancer
出处 《实用医学杂志》 CAS 北大核心 2017年第18期2983-2986,共4页 The Journal of Practical Medicine
基金 江西省卫生计生委科技计划项目(编号:20171113)
关键词 乳腺肿瘤 组织型转谷氨酰胺酶 耐药 表阿霉素 breast cancer TG2 drug resistance epirubicin
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