TG2 promotes drug resistance to epirubicin through AKT signal pathway in breast cancer
10.3969/j.issn.1006-5725.2017.18.002
- VernacularTitle:TG2通过AKT通路调节乳腺癌对表阿霉素耐药性
- Author:
Dongmei LI
1
;
Wenxing HE
;
Zhengkui SUN
;
Weiying XU
;
Guanglan LU
Author Information
1. 江西省肿瘤医院乳腺科
- Keywords:
breast cancer;
TG2;
drug resistance;
epirubicin
- From:
The Journal of Practical Medicine
2017;33(18):2983-2986
- CountryChina
- Language:Chinese
-
Abstract:
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. MTT 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
