Evidence map›Paper›PMID 40956032›Full record

ReviewCancer medicine2025

Metabolic Reprogramming of Cancer Cells and Therapeutics Targeting Cancer Metabolism.

Jilsy M J Punnasseril, Abdul Auwal, Vinod Gopalan, Alfred King-Yin Lam, Farhadul Islam

Abstract readReview
In one paragraph

Review in Cancer medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
–field-weighted citation impact
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

19 citing papers in PubMed.

  1. Article
  2. Histone deacetylases in cancer metabolic reprogramming.Experimental & molecular medicine · 2026
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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

5 authors.

Jilsy M J PunnasserilSchool of Medicine & Dentistry, Griffith University, Gold Coast Campus, Southport, Queensland, Australia.
Abdul AuwalDepartment of Biochemistry & Molecular Biology, Rajshahi University, Rajshahi, Bangladesh.
Vinod GopalanSchool of Medicine & Dentistry, Griffith University, Gold Coast Campus, Southport, Queensland, Australia.
Alfred King-Yin LamSchool of Medicine & Dentistry, Griffith University, Gold Coast Campus, Southport, Queensland, Australia.ORCID https://orcid.org/0000-0003-2771-564X
Farhadul IslamSchool of Medicine & Dentistry, Griffith University, Gold Coast Campus, Southport, Queensland, Australia.ORCID https://orcid.org/0000-0001-5262-4702

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCancer metabolism is a field focused on the unique alterations in metabolic pathways that occur in cancer cells, distinguishing them from the metabolic processes in normal cells.

methodsAn extensive review of the current literature on the metabolic adaptation of cancer cells was carried out in the current study.

resultsThe rapidly proliferating cells require high levels of molecules, such as glucose, amino acids, lipids, and nucleotides, along with increased energy demand (ATP). These requirements are met through alterations in the processes involving glucose, amino acid, lipid, and nucleotide metabolism. Modifications in glucose metabolism in cancer cells involve changes in glucose uptake, glycolysis, the pentose phosphate pathway, and the tricarboxylic acid cycle. Similarly, alterations in amino acid metabolism in cancer cells relate to upregulated amino acid transport and glutaminolysis. Cancer cells also have increased lipid intake from the extracellular microenvironment, upregulated lipogenesis, and enhanced lipid storage and mobilization from intracellular lipid droplets. These rapidly proliferating cells also achieve their increased demand for nucleotides by changing the expression of enzymes in the salvage and de novo nucleotide pathways. Consequently, these metabolic processes are targets for developing cancer therapeutics. However, it is important to note that the metabolic changes in cancer cells can also contribute to resistance against various cancer therapies.

conclusionThis review will explore the various ways in which cancer cells reprogram metabolic processes to sustain rapid proliferation and survival. The information presented in this report could help in the therapeutics designed to target them, and the challenges of cancer drug resistance arising from these metabolic adaptations.

Indexed as

Antineoplastic AgentsEnergy MetabolismNeoplasmsAnimalsGlucoseGlycolysisHumansLipid MetabolismMetabolic ReprogrammingTumor MicroenvironmentAntineoplastic AgentsGlucosecancer metabolismdrug resistanceglucose metabolismnucleotide metabolismtherapeuticsWarburg effect

Identifiers

PMID40956032
PMCPMC12439291

What OpenQuestion holds

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Registered trials

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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.