Actin-sequestering protein, thymosin beta-4, induces paclitaxel resistance through ROS/HIF-1alpha stabilization in HeLa human cervical tumor cells

Life Sciences
Jin-Mi Oh, Eun-Yi Moon

Abstract

We investigated whether actin-sequestering protein, thymosin beta-4 (TB4)-induced reactive oxygen species (ROS) affect the stabilization of hypoxia-inducible transcription factor (HIF)-1alpha and paclitaxel-resistance induction. HeLa human cervical tumor cells were used. The percentage of cell survival was determined by MTT assay. ROS production, cell cycle and hypodiploid cell formation were assessed by flow cytometry analysis. HIF-1alpha stabilization and molecular changes were analyzed by western blotting or RT-PCR. NF-kappaB activation was assessed by EMSA and western blotting. TB4 protein (TB4P) significantly increased intracellular ROS level and HIF-1alpha. The increased level of HIF-1alpha by TB4P was reduced by the treatment with N-acetylcysteine (NAC), a well-known ROS scavenger. TB4P-induced ROS production was confirmed by the activation of nuclear factor kappa B. TB4P-induced Erk phosphorylation was attenuated by the treatment with NAC. In addition, tumor cell death was decreased by TB4 gene overexpression and TB4P treatment. NAC treatment attenuated tumor cell density increased by TB4P. Tumor cell death by paclitaxel was also increased by NAC treatment or the transfection with HIF-1alpha-siRNA. Paclitaxel-induced B1...Continue Reading

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Citations

Jan 17, 2013·Cancer Investigation·Sirinapa SribenjaChangyi Chen
Feb 7, 2012·Veterinary Parasitology·Yun-Jeong KangMee Sun Ock
Nov 15, 2018·Journal of Cellular Biochemistry·Safieh EbrahimiSeyed Isaac Hashemy
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