Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0017636 (glioblastoma)
 18,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypoxia-induced alterations in the cellular redox status play a critical role in the development of hypoxia-induced chemoresistance in cancer cells. Human biliverdin reductase (hBVR), an enzyme involved in the conversion of biliverdin into bilirubin in heme metabolism, was recently identified as an important cytoprotectant against oxidative stress and hypoxia. However, the role of hBVR on hypoxia-induced drug resistance has not been previously investigated. Using human glioblastoma cell lines, we evaluated the potential role of hBVR in hypoxia-induced drug resistance. We found that hypoxia caused a significant increase in hBVR expression in glioblastoma cells that was accompanied by chemoresistance. We also observed that siRNA-based targeting of hBVR genes attenuated the hypoxia-induced chemoresistance. Furthermore, knocking down hBVR induced a marked increase in the levels of intracellular reactive oxygen species under hypoxic conditions, and the chemosensitizing effect of hBVR depletion was reversed by pretreatment with the antioxidant N-acetylcysteine. These findings suggest that hBVR significantly contributes to the modulation of hypoxia-induced chemoresistance of glioblastoma cells by adjusting their cellular redox status.
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PMID:Biliverdin reductase plays a crucial role in hypoxia-induced chemoresistance in human glioblastoma. 2411 78