JNK,p-JNK 南京医科大学(英文版).pdfVIP

Apoptosis DOI 10.1007/s10495-011-0637-6 ORIGINAL PAPER JWA enhances As O -induced tubulin polymerization 2 3 and apoptosis via p38 in HeLa and MCF-7 cells Lianlian Shen • Wenxia Xu • Aiping Li • Jian Ye • Jianwei Zhou Springer Science+Business Media, LLC 2011 Abstract Arsenic trioxide (As O ) has potential anti- effective in solid tumor cells [2, 3]. Thus, there was an 2 3 cancer activity against a wide range of carcinomas via increasing interest in discovering the full range of arsenic’s apoptosis induction or oncoprotein degradation. The potential as a chemotherapeutic agent and several clinical mechanisms involved are not fully elucidated. Here, we trials have been initiated to test the efficacy of arsenic in demonstrated that As2O3 induced-apoptosis in HeLa and treating solid tumours. We chose two cell lines HeLa MCF-7 cancer cells was in part triggered by tubulin poly- (relatively sensitive to As O ) and MCF-7 (relatively 2 3 merization. High expression of JWA promoted tubulin resistant to As O ) to investigate the molecular mecha- 2 3 polymerization and increased the sensitivity of the cancer nisms involved in As O -induced apoptosis. Published data 2 3 cells to As O . The activation of the p38 MAPK (mitogen- has shown that reactive oxygen species (ROS) may be 2 3 activated protein kinases) signaling pathway was found to