Evidence map›Paper›PMID 40919131›Full record

ReviewMedComm2025

Metabolic Reprogramming: A Crucial Contributor to Anticancer Drug Resistance.

Yunhan Zhu, Weijie Yan, Lingfeng Tong, Jie Yang, Shengfang Ge, Jiayan Fan, Renbing Jia, Xuyang Wen

Abstract readReview
In one paragraph

Review in MedComm, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing 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

21 citing papers in PubMed.

  1. Article
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  4. Targeting metabolic dependencies to reverse chemoradiotherapy resistance in colorectal cancer.Journal of experimental & clinical cancer research : CR · 2026
    Article
  5. Review
  6. Leveraging Macrophage Metabolic Reprogramming for Enhanced Anti-Tumor Immunity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Review
  7. Review
  8. Article
  9. Article
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  12. Article
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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

8 authors.

Yunhan ZhuDepartment of Ophthalmology Ninth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine Shanghai China.
Weijie YanDepartment of Ophthalmology Ninth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine Shanghai China.
Lingfeng TongEngineering Research Center of Techniques and Instruments for Diagnosis and Treatment of Congenital Heart Disease, Ministry of Education Xinhua Hospital, Shanghai Jiao Tong University School of Medicine Shanghai China.
Jie YangDepartment of Ophthalmology Ninth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine Shanghai China.
Shengfang GeDepartment of Ophthalmology Ninth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine Shanghai China.
Jiayan FanDepartment of Ophthalmology Ninth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine Shanghai China.
Renbing JiaDepartment of Ophthalmology Ninth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine Shanghai China.
Xuyang WenDepartment of Ophthalmology Ninth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine Shanghai China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer metabolic reprogramming is a fundamental hallmark that enables tumor cells to sustain their malignant behaviors. Beyond its role in supporting growth, invasion, and migration, metabolic rewiring actively contributes to anticancer drug resistance. Cancer cells not only reshape their own metabolism but also engage in aberrant metabolic crosstalk with nonmalignant components within the tumor microenvironment (TME). These metabolic alterations create multiple barriers to the efficacy of drug therapies, including chemotherapy, targeted therapy, and immunotherapy. Despite growing evidence, an integrated understanding of how metabolic reprogramming contributes to the development of drug resistance and how it may be therapeutically targeted to overcome the resistance remains incomplete. This review summarizes recent progresses in tumor-intrinsic and TME-associated metabolic alterations that contribute to drug resistance by sustaining metabolic needs and modulating nonmetabolic processes and explores the upstream regulatory mechanisms driving these changes, focusing particularly on glucose, lipid, and amino acid metabolism. We also discuss the current advances in the integration of small molecule inhibitors targeting cancer metabolism to address drug resistance. By consolidating mechanistic insights and therapeutic opportunities, this review highlights metabolic reprogramming as a promising intervention point to overcome anticancer drug resistance.

Indexed as

cancer metabolismdrug resistancemetabolic targeted strategiestumor microenvironment

Identifiers

PMID40919131
PMCPMC12413565

What OpenQuestion holds

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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.