Abstract：
UNASSIGNED: Microwave ablation (MWA) is a widely adopted treatment technique for hepatocellular carcinoma (HCC). However, MWA alone is of limited use and has a high recurrence rate. Transforming growth factor-β1 (TGF-β1) is recognized as a potential therapeutic target for HCC patients. Therefore, this study was designed to investigate whether the TGF-β1 inhibitor could increase the efficacy of MWA therapy for HCC treatment.
UNASSIGNED: In vitro, HCC cells challenged with TGF-β1 inhibitor (SB-525334), or normal saline were then heated by microwave. Methyl tetrazolium assays were performed to detect cell survival rate and half-maximal drug inhibitory concentration (IC50). Cell viability and apoptosis were detected by cell counting kit-8 assays, flow cytometry and western blotting. In vivo, the mice injected with HepG2 cells received oral gavage of SB-525334 (20 mg/kg) or normal saline and MWA at a power of 15 W. Tumor volume was recorded. Expression of Ki67 and apoptosis-related proteins were detected by immunohistochemistry and western blotting. TUNEL assays were used to detect cell death ratio. Histopathological changes were examined by hematoxylin and eosin staining. The mechanisms associated with the function of MWA combined with TGF-β1 inhibitor in HCC development were explored by western blotting.
UNASSIGNED: Combination of MWA and SB-525334 decreased the survival rate and promoted the apoptosis of HCC cells compared with MWA alone. SB-525334 enhanced the suppressive effect of MWA on tumor growth and amplified cell apoptosis. Mechanistically, MWA collaborated with SB-525334 inhibitor inactivated the TGF-β1/Smad2/Smad3 pathway.
UNASSIGNED: TGF-β1 inhibitor enhances the therapeutic effect of MWA on HCC.
UNASSIGNED: In vitro, HCC cells challenged with TGF-β1 inhibitor (SB-525334), or normal saline were then heated by microwave. Methyl tetrazolium assays were performed to detect cell survival rate and half-maximal drug inhibitory concentration (IC50). Cell viability and apoptosis were detected by cell counting kit-8 assays, flow cytometry and western blotting. In vivo, the mice injected with HepG2 cells received oral gavage of SB-525334 (20 mg/kg) or normal saline and MWA at a power of 15 W. Tumor volume was recorded. Expression of Ki67 and apoptosis-related proteins were detected by immunohistochemistry and western blotting. TUNEL assays were used to detect cell death ratio. Histopathological changes were examined by hematoxylin and eosin staining. The mechanisms associated with the function of MWA combined with TGF-β1 inhibitor in HCC development were explored by western blotting.
UNASSIGNED: Combination of MWA and SB-525334 decreased the survival rate and promoted the apoptosis of HCC cells compared with MWA alone. SB-525334 enhanced the suppressive effect of MWA on tumor growth and amplified cell apoptosis. Mechanistically, MWA collaborated with SB-525334 inhibitor inactivated the TGF-β1/Smad2/Smad3 pathway.
UNASSIGNED: TGF-β1 inhibitor enhances the therapeutic effect of MWA on HCC.
摘要：
■微波消融（MWA）是一种广泛采用的肝细胞癌（HCC）治疗技术。然而,单独使用MWA是有限的并且具有高复发率。转化生长因子-β1（TGF-β1）被认为是HCC患者的潜在治疗靶标。因此,本研究旨在探讨TGF-β1抑制剂是否能提高MWA治疗HCC的疗效.
■体外，用TGF-β1抑制剂（SB-525334）攻击的肝癌细胞，或生理盐水用微波加热。进行甲基四唑盐测定以检测细胞存活率和半数最大药物抑制浓度(IC50)。细胞计数试剂盒-8法检测细胞活力和凋亡,流式细胞术和蛋白质印迹。在体内,注射HepG2细胞的小鼠接受SB-525334(20mg/kg)或生理盐水和MWA的口服灌胃,功率为15W。免疫组织化学和免疫印迹法检测Ki67和凋亡相关蛋白的表达。TUNEL测定用于检测细胞死亡比率。通过苏木精和伊红染色检查组织病理学变化。通过蛋白质印迹法探讨了MWA联合TGF-β1抑制剂在HCC发展中的作用机制。
■与单独使用MWA相比，MWA和SB-525334的组合降低了HCC细胞的存活率并促进了凋亡。SB-525334增强了MWA对肿瘤生长的抑制作用并放大了细胞凋亡。机械上,MWA与SB-525334抑制剂合作灭活了TGF-β1/Smad2/Smad3途径。
■TGF-β1抑制剂增强MWA对HCC的治疗作用。
■体外，用TGF-β1抑制剂（SB-525334）攻击的肝癌细胞，或生理盐水用微波加热。进行甲基四唑盐测定以检测细胞存活率和半数最大药物抑制浓度(IC50)。细胞计数试剂盒-8法检测细胞活力和凋亡,流式细胞术和蛋白质印迹。在体内,注射HepG2细胞的小鼠接受SB-525334(20mg/kg)或生理盐水和MWA的口服灌胃,功率为15W。免疫组织化学和免疫印迹法检测Ki67和凋亡相关蛋白的表达。TUNEL测定用于检测细胞死亡比率。通过苏木精和伊红染色检查组织病理学变化。通过蛋白质印迹法探讨了MWA联合TGF-β1抑制剂在HCC发展中的作用机制。
■与单独使用MWA相比，MWA和SB-525334的组合降低了HCC细胞的存活率并促进了凋亡。SB-525334增强了MWA对肿瘤生长的抑制作用并放大了细胞凋亡。机械上,MWA与SB-525334抑制剂合作灭活了TGF-β1/Smad2/Smad3途径。
■TGF-β1抑制剂增强MWA对HCC的治疗作用。
