Bao 2021 Cells: Difference between revisions

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{{Publication
{{Publication
|title=Bao MH, Wong CC (2021) Hypoxia, metabolic reprogramming, and drug resistance in liver cancer. Cells 10:1715. doi: 10.3390/cells10071715
|title=Bao MH, Wong CC (2021) Hypoxia, metabolic reprogramming, and drug resistance in liver cancer. Cells 10:1715. https://doi.org/10.3390/cells10071715
|info=[https://pubmed.ncbi.nlm.nih.gov/34359884/ PMID: 34359884 Open Access]
|info=[https://pubmed.ncbi.nlm.nih.gov/34359884/ PMID: 34359884 Open Access]
|authors=Bao MH, Wong CC
|authors=Bao MH, Wong CC
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|editor=Gnaiger E
|editor=Gnaiger E
}}
}}
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{{Template:Correction FADH2 and S-pathway}}
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{{Labeling
|enzymes=Complex II;succinate dehydrogenase
|enzymes=Complex II;succinate dehydrogenase
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[[File:Bao 2021 Cells CORRECTION.png|right|400px]]
{{Template:Correction FADH2 and S-pathway}}

Latest revision as of 23:08, 23 April 2023

Publications in the MiPMap
Bao MH, Wong CC (2021) Hypoxia, metabolic reprogramming, and drug resistance in liver cancer. Cells 10:1715. https://doi.org/10.3390/cells10071715

Β» PMID: 34359884 Open Access

Bao MH, Wong CC (2021) Cells

Abstract: Hypoxia, low oxygen (O2) level, is a hallmark of solid cancers, especially hepatocellular carcinoma (HCC), one of the most common and fatal cancers worldwide. Hypoxia contributes to drug resistance in cancer through various molecular mechanisms. In this review, we particularly focus on the roles of hypoxia-inducible factor (HIF)-mediated metabolic reprogramming in drug resistance in HCC. Combination therapies targeting hypoxia-induced metabolic enzymes to overcome drug resistance will also be summarized. Acquisition of drug resistance is the major cause of unsatisfactory clinical outcomes of existing HCC treatments. Extra efforts to identify novel mechanisms to combat refractory hypoxic HCC are warranted for the development of more effective treatment regimens for HCC patients.

β€’ Bioblast editor: Gnaiger E

Bao 2021 Cells CORRECTION.png

Correction: FADH2 and Complex II

Ambiguity alert.png
FADH2 is shown as the substrate feeding electrons into Complex II (CII). This is wrong and requires correction - for details see Gnaiger (2024).
Gnaiger E (2024) Complex II ambiguities ― FADH2 in the electron transfer system. J Biol Chem 300:105470. https://doi.org/10.1016/j.jbc.2023.105470 - Β»Bioblast linkΒ«


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Enzyme: Complex II;succinate dehydrogenase 




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