Treatment with MG-132 and TSA induced apoptosis in OS-RC-2 cells by increasing oxidative stress and decreasing the expression of NF- kappa B

MIQING XU (Department of Geriatrics, Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, China)
HUI XIE (Department of Geriatrics, Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, China)
YUN ZHONG (Guangzhou Institute of Cardiovascular Disease, Guangzhou, China)
JUNJIAN MA (Department of Geriatrics, Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, China)
SHIMING LIU (3Guangzhou Institute of Cardiovascular Disease, Guangzhou, China)
HUI YANG (Department of Gastroenterology, Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, China)

Nusantara Bioscience
Vol. 7 No. 1 (2015)

Abstract. Xu M, Xie H, Zhong Y, Ma J, Liu S, Yang H. 2015. Treatment with MG-132 and TSA induced apoptosis in OS-RC-2 cells by increasing oxidative stress and decreasing the expression of NF-kappa B. Nusantara Bioscience 7: 20-25. Here we assessed the effect of the proteasome inhibitor MG-132 alone or in combination with the histone deacetylase inhibitor TSA on human renal cell on human renal cell carcinoma cells in vitro and we explored the underlying molecular mechanisms.OS-RC-2 cells were treated byMG-132 alone or in combination with TSA and/or NAc. The MTT assay and flow cytometry (FCM) were used to determine cell viability, ROS levels, and apoptosis. Expression of Bax and NF-kappa B p65 proteins was quantified by Western blotting. MG-132significantly increased the level of ROS, inhibited cell growth and induced apoptosis in a dose- and time-dependent manner. Both ROS and apoptosis were further increased following the combined addition of MG132 and TSA. In all cases, expression of p65 was down-regulated. MG-132 alone or in combination with TSA induced apoptosis in OS-RC-2 cells through the generation of ROS and the down-regulation of p65 expression.