RESUMO
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
RESUMO
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
RESUMO
Objective To review the mechanisms of breast cancer escaping from host immune surveillance. Methods The current literatures on the mechanisms of breast cancer cells escaping from host immune surveillance were reviewed in the following aspects: alterations of MHC-Ⅰmolecule phenotype, deficiency of costimulatory molecules, apoptosis of T-lymphocytes induced by breast cancer cells presenting Fas ligand (FasL) and TNF-related apoptosis-inducing ligand (TRAIL) and host immune tolerance induced by tumor cells. Results Loss of classical antigen-presenting human leukocyte antigen (HLA) class-Ⅰmolecules, expression of non-classical HLA class-ⅠmoleculesHLA-G, loss of costimulatory molecule B7, apoptosis of T-lymphocytes induced by tumor cells presenting FasL and TRAIL and antigen-inducing host immune tolerance were related to breast cancer escaping from immune surveillance. Conclusion Breast cancer cells escape from host immune surveillance by altering MHC-Ⅰmolecules, lacking of costimulatory molecules, inducing of apoptosis of T cells and host immune tolerance. But the factors resulting in breast cancer escaping from host immune surveillance are not yet clear and should be further studied.