Evidence map›Paper›PMID 38139067›Full record

ReviewInternational journal of molecular sciences2023

The Emerging Roles of the Metabolic Regulator G6PD in Human Cancers.

Alfar Ahamed, Rendy Hosea, Shourong Wu, Vivi Kasim

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
15.7field-weighted citation impact, top 1% 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

28 citing papers in PubMed, 27 citations in OpenAlex.

  1. Review
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  11. The Yin-Yang balance of SIRT1 and SIRT2 in cancer metabolic remodeling.International journal of biological sciences · 2026
    Review
  12. Safety and probiotic characterization ofFrontiers in microbiology · 2026
    Article
  13. Review
  14. Review
  15. Article
  16. Advances in Molecular and Translational Medicine: 2nd Edition.International journal of molecular sciences · 2025
    Article
  17. Article
  18. Article
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  20. Review
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

4 authors at 1 institution in 1 country.

Alfar AhamedKey Laboratory of Biorheological Science and Technology of Ministry of Education, College of Bioengineering, Chongqing University, Chongqing 400045, China.ORCID 0009-0005-4914-5694
Rendy HoseaKey Laboratory of Biorheological Science and Technology of Ministry of Education, College of Bioengineering, Chongqing University, Chongqing 400045, China.ORCID 0000-0003-3883-9613
Shourong WuKey Laboratory of Biorheological Science and Technology of Ministry of Education, College of Bioengineering, Chongqing University, Chongqing 400045, China.ORCID 0000-0001-9650-5465
Vivi KasimKey Laboratory of Biorheological Science and Technology of Ministry of Education, College of Bioengineering, Chongqing University, Chongqing 400045, China.ORCID 0000-0001-9182-8230
Chongqing University · CN

Funding

National Natural Science Foundation of China 32070715National Natural Science Foundation of China 32270778National Natural Science Foundation of China 81872273National Natural Science Foundation of China 82173029Natural Science Foundation of Chongqing CSTB2022NSCQ-MSX0611Natural Science Foundation of Chongqing CSTB2022NSCQ-MSX0612
6 · The paper itself

Abstract

Metabolic reprogramming, especially reprogrammed glucose metabolism, is a well-known cancer hallmark related to various characteristics of tumor cells, including proliferation, survival, metastasis, and drug resistance. Glucose-6-phosphate dehydrogenase (G6PD) is the first and rate-limiting enzyme of the pentose phosphate pathway (PPP), a branch of glycolysis, that converts glucose-6-phosphate (G6P) into 6-phosphogluconolactone (6PGL). Furthermore, PPP produces ribose-5-phosphate (R5P), which provides sugar-phosphate backbones for nucleotide synthesis as well as nicotinamide adenine dinucleotide phosphate (NADPH), an important cellular reductant. Several studies have shown enhanced G6PD expression and PPP flux in various tumor cells, as well as their correlation with tumor progression through cancer hallmark regulation, especially reprogramming cellular metabolism, sustaining proliferative signaling, resisting cell death, and activating invasion and metastasis. Inhibiting G6PD could suppress tumor cell proliferation, promote cell death, reverse chemoresistance, and inhibit metastasis, suggesting the potential of G6PD as a target for anti-tumor therapeutic strategies. Indeed, while challenges-including side effects-still remain, small-molecule G6PD inhibitors showing potential anti-tumor effect either when used alone or in combination with other anti-tumor drugs have been developed. This review provides an overview of the structural significance of G6PD, its role in and regulation of tumor development and progression, and the strategies explored in relation to G6PD-targeted therapy.

Indexed as

Glucosephosphate DehydrogenaseNeoplasmsAnimalsGlycolysisHumansPentose Phosphate PathwayG6PD protein, humanGlucosephosphate Dehydrogenaseanti-tumor therapydrug resistanceglucose-6-phosphate dehydrogenase (G6PD)pentose phosphate pathway (PPP)tumor cell proliferationtumor metabolism

Identifiers

PMID38139067
PMCPMC10743588
OpenAlexW4389433059

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.