Hypoxia-inducible transcription factor (HIF)-1α stabilization by actin-sequestering protein, thymosin beta-4 (TB4) in Hela cervical tumor cells
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- Hypoxia-inducible transcription factor (HIF)-1α stabilization by actin-sequestering protein, thymosin beta-4 (TB4) in Hela cervical tumor cells
- J M Oh; In Ja Ryoo; Y Yang; H S Kim; K H Yang; E Y Moon
- Bibliographic Citation
- Cancer Letters, vol. 264, no. 1, pp. 29-35
- Publication Year
- Thymosin beta-4 (TB4) is an actin-sequestering protein to control cytoskeletal reorganization. Here, we investigated whether TB4 proteins (TB4P) affect tumor microenvironment by measuring hypoxia-inducible transcription factor (HIF)-1α stabilization in cervical tumor cells, since TB4P reduced paclitaxel-induced cell death rate. TB4P increased HIF-1α stabilization and transactivation, which is measured by the increase of hypoxia response element (HRE)-luciferase activity and target gene, vascular endothelial growth factor (VEGF) transcription. TB4P also elevated ERK phosphorylation. PD98059, ERK inhibitor reduced HIF-1α increased by TB4P. Paclitaxel-induced cell death was inhibited by hypoxia conditioning that increased HIF-1α stabilization and ERK phosphorylation. PD98059 reversed paclitaxel-induced cell death which was attenuated by hypoxia. Collectively, TB4P could lead tumor cell microenvironment to hypoxia condition, which might be resulted in antitumor drug-resistance induction. It suggests that soluble TB4P could be a novel target to control tumor cell death by regulating tumor cell microenvironment.
- ERK; Hela cell; HIF-1α; Hypoxia; Thymosin beta-4
- Appears in Collections:
- Ochang Branch Institute > Anticancer Agent Research Center > 1. Journal Articles
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