Evidence map›Paper›PMID 33291643›Full record

ReviewCells2020

Hypoxia Dictates Metabolic Rewiring of Tumors: Implications for Chemoresistance.

Dimas Carolina Belisario, Joanna Kopecka, Martina Pasino, Muhlis Akman, Enrico De Smaele, Massimo Donadelli, Chiara Riganti

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed, 1 pooled it
5.3field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

80 citing papers in PubMed, 1 synthesis or guideline pooled it, 119 citations in OpenAlex.

  1. Pooled it
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  5. Article
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  10. Bioelectronics forNanotheranostics · 2026
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  11. Article
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  13. Article
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  15. Sonodynamic biomimetic-nanomedicine fight cancers.Journal of nanobiotechnology · 2025
    Review
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  19. ALKBH3-regulated mActa pharmaceutica Sinica. B · 2025
    Article
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20 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 1 country.

Dimas Carolina BelisarioDepartment of Oncology, University of Torino, via Santena 5/bis, 10126 Torino, Italy.
Joanna KopeckaDepartment of Oncology, University of Torino, via Santena 5/bis, 10126 Torino, Italy.ORCID 0000-0003-3612-3953
Martina PasinoDepartment of Oncology, University of Torino, via Santena 5/bis, 10126 Torino, Italy.
Muhlis AkmanDepartment of Oncology, University of Torino, via Santena 5/bis, 10126 Torino, Italy.
Enrico De SmaeleDepartment of Experimental Medicine, Sapienza University of Roma, 00185 Roma, Italy.
Massimo DonadelliDepartment of Neurosciences, Biomedicine and Movement Sciences, Section of Biochemistry, University of Verona, 37134 Verona, Italy.ORCID 0000-0001-9224-9230
Chiara RigantiDepartment of Oncology, University of Torino, via Santena 5/bis, 10126 Torino, Italy.ORCID 0000-0001-9787-4836
University of Turin · ITSapienza University of Rome · ITUniversity of Verona · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypoxia is a condition commonly observed in the core of solid tumors. The hypoxia-inducible factors (HIF) act as hypoxia sensors that orchestrate a coordinated response increasing the pro-survival and pro-invasive phenotype of cancer cells, and determine a broad metabolic rewiring. These events favor tumor progression and chemoresistance. The increase in glucose and amino acid uptake, glycolytic flux, and lactate production; the alterations in glutamine metabolism, tricarboxylic acid cycle, and oxidative phosphorylation; the high levels of mitochondrial reactive oxygen species; the modulation of both fatty acid synthesis and oxidation are hallmarks of the metabolic rewiring induced by hypoxia. This review discusses how metabolic-dependent factors (e.g., increased acidification of tumor microenvironment coupled with intracellular alkalinization, and reduced mitochondrial metabolism), and metabolic-independent factors (e.g., increased expression of drug efflux transporters, stemness maintenance, and epithelial-mesenchymal transition) cooperate in determining chemoresistance in hypoxia. Specific metabolic modifiers, however, can reverse the metabolic phenotype of hypoxic tumor areas that are more chemoresistant into the phenotype typical of chemosensitive cells. We propose these metabolic modifiers, able to reverse the hypoxia-induced metabolic rewiring, as potential chemosensitizer agents against hypoxic and refractory tumor cells.

Indexed as

Drug Resistance, NeoplasmAmino AcidsAnimalsCitric Acid CycleDimerizationDisease ProgressionEpithelial-Mesenchymal TransitionGlucoseGlutamineHumansHypoxiaLactic AcidMiceMitochondriaNeoplasmsOxidation-ReductionAmino AcidsGlucoseGlutamineLactic AcidOxygenReactive Oxygen Speciescancerchemoresistancehypoxiametabolic reprogramming

Identifiers

PMID33291643
PMCPMC7761956
OpenAlexW3109893680

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.