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Hypoxia-inducible transcription factor (HIF)-1α stabilization by actin-sequestering protein, thymosin beta-4 (TB4) in Hela cervical tumor cells

Authors
  • ryoo, in ja
  • yang, y
  • kim, h s
  • yang, k h
  • e moon, y
Publication Date
Jan 01, 2008
Identifiers
DOI: 10.1016/j.canlet.2008.01.004
OAI: oai:https://repository.kribb.re.kr:201005/8426
Source
KRIBB Repository
Keywords
License
Unknown
External links

Abstract

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. / open

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