Huang Yunxiu, Su Min, Wei Lan, Ji Feihu, Wang Nian, Zhong Changli, Chen Tingmei
Ministry of Education Key Laboratory of Laboratory Medical Diagnostics, Chongqing Medical University, Chongqing 400016, China.
Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. 2015 Nov;31(11):1458-62.
To investigate the effect of NF-κB inhibitor BAY11-7082 on proliferation and apoptosis of breast carcinoma MCF-7 cells and the underlying mechanism.
MCF-7 cells in the logarithmic growth phase were divided into control group, 5 μmol/L BAY11-7082 group and 10 μmol/L LY294002 group. After the treatment of BAY11-7082 and LY294002, the protein levels of ATP citrate lyase (ACL), phosphated-ACL (p-ACL), phosphated-Akt (p-Akt) and phosphated nuclear factor κB (p-NF-κB) were determined by Western blotting. The proliferation of MCF-7 cells treated with BAY11-7082 or siACL were detected by CCK-8 assay. The apoptosis of MCF-7 cells treated with BAY11-7082 or siACL were observed by flow cytometry combined with annexin V-FITC/PI staining.
The proliferation of MCF-7 cells was inhibited by BAY11-7082 in a dose-dependent manner. Compared with the control group, the expressions of p-ACL and p-NF-κB protein in MCF-7 cells treated with BAY11-7082 were lowered. The expressions of p-ACL and p-NF-κB protein in MCF-7 cells treated with 10 μmol/L LY294002 were also reduced significantly. The proliferation of MCF-7 cells treated with BAY11-7082 or siACL for 48 hours was inhibited and the apoptosis was promoted significantly, as shown by CCK-8 assay and flow cytometry.
BAY11-7082 could inhibit the proliferation of MCF-7 breast carcinoma cells and promote the apoptosis by inhibiting the phosphorylation of ACL.
探讨核因子κB（NF-κB）抑制剂BAY11-7082对乳腺癌MCF-7细胞增殖和凋亡的影响及其潜在机制。
将对数生长期的MCF-7细胞分为对照组、5 μmol/L BAY11-7082组和10 μmol/L LY294002组。经BAY11-7082和LY294002处理后，采用蛋白质免疫印迹法检测三磷酸腺苷柠檬酸裂解酶（ACL）、磷酸化ACL（p-ACL）、磷酸化蛋白激酶B（p-Akt）和磷酸化核因子κB（p-NF-κB）的蛋白水平。采用细胞计数试剂盒-8（CCK-8）法检测经BAY11-7082或小干扰RNA（siACL）处理的MCF-7细胞的增殖情况。采用流式细胞术结合膜联蛋白V-异硫氰酸荧光素/碘化丙啶（annexin V-FITC/PI）染色观察经BAY11-7082或siACL处理的MCF-7细胞的凋亡情况。
BAY11-7082以剂量依赖的方式抑制MCF-7细胞的增殖。与对照组相比，经BAY11-7082处理的MCF-7细胞中p-ACL和p-NF-κB蛋白的表达降低。经10 μmol/L LY294002处理的MCF-7细胞中p-ACL和p-NF-κB蛋白的表达也显著降低。CCK-8法和流式细胞术结果显示，经BAY11-7082或siACL处理48小时后，MCF-7细胞的增殖受到抑制，凋亡明显增加。
BAY11-7082可通过抑制ACL的磷酸化来抑制MCF-7乳腺癌细胞的增殖并促进其凋亡。
