PMID- 35432450
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220510
IS  - 1664-8021 (Print)
IS  - 1664-8021 (Electronic)
IS  - 1664-8021 (Linking)
VI  - 13
DP  - 2022
TI  - Therapeutic Targeting Hypoxia-Inducible Factor (HIF-1) in Cancer: Cutting Gordian 
      Knot of Cancer Cell Metabolism.
PG  - 849040
LID - 10.3389/fgene.2022.849040 [doi]
LID - 849040
AB  - Metabolic alterations are one of the hallmarks of cancer, which has recently 
      gained great attention. Increased glucose absorption and lactate secretion in 
      cancer cells are characterized by the Warburg effect, which is caused by the 
      metabolic changes in the tumor tissue. Cancer cells switch from oxidative 
      phosphorylation (OXPHOS) to aerobic glycolysis due to changes in glucose 
      degradation mechanisms, a process known as "metabolic reprogramming". As a 
      result, proteins involved in mediating the altered metabolic pathways identified 
      in cancer cells pose novel therapeutic targets. Hypoxic tumor microenvironment 
      (HTM) is anticipated to trigger and promote metabolic alterations, oncogene 
      activation, epithelial-mesenchymal transition, and drug resistance, all of which 
      are hallmarks of aggressive cancer behaviour. Angiogenesis, erythropoiesis, 
      glycolysis regulation, glucose transport, acidosis regulators have all been 
      orchestrated through the activation and stability of a transcription factor 
      termed hypoxia-inducible factor-1 (HIF-1), hence altering crucial Warburg effect 
      activities. Therefore, targeting HIF-1 as a cancer therapy seems like an 
      extremely rational approach as it is directly involved in the shift of cancer 
      tissue. In this mini-review, we present a brief overview of the function of HIF-1 
      in hypoxic glycolysis with a particular focus on novel therapeutic strategies 
      currently available.
CI  - Copyright (c) 2022 Sharma, Sinha and Shrivastava.
FAU - Sharma, Abhilasha
AU  - Sharma A
AD  - Department of Life Science, University School of Sciences, Gujarat University, 
      Ahmedabad, India.
FAU - Sinha, Sonam
AU  - Sinha S
AD  - Kashiv Biosciences, Ahmedabad, India.
FAU - Shrivastava, Neeta
AU  - Shrivastava N
AD  - Shri B.V. Patel Education Trust, Ahmedabad, India.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20220331
PL  - Switzerland
TA  - Front Genet
JT  - Frontiers in genetics
JID - 101560621
PMC - PMC9008776
OTO - NOTNLM
OT  - cancer
OT  - cancer therapies
OT  - clinical outcomes
OT  - genomic alterations
OT  - hypoxia-induced tumor microenvironment
OT  - metabolic reprogramming
OT  - metabolism
OT  - warburg effect
COIS- SS was employed by the company Kashiv Biosciences. The remaining authors declare 
      that the research was conducted in the absence of any commercial or financial 
      relationships that could be construed as a potential conflict of interest.
EDAT- 2022/04/19 06:00
MHDA- 2022/04/19 06:01
PMCR- 2022/03/31
CRDT- 2022/04/18 06:34
PHST- 2022/01/05 00:00 [received]
PHST- 2022/03/09 00:00 [accepted]
PHST- 2022/04/18 06:34 [entrez]
PHST- 2022/04/19 06:00 [pubmed]
PHST- 2022/04/19 06:01 [medline]
PHST- 2022/03/31 00:00 [pmc-release]
AID - 849040 [pii]
AID - 10.3389/fgene.2022.849040 [doi]
PST - epublish
SO  - Front Genet. 2022 Mar 31;13:849040. doi: 10.3389/fgene.2022.849040. eCollection 
      2022.