Evidence map›Paper›PMID 40884151›Full record

ReviewCancer medicine2025

Glucose Metabolic Reprogramming in Colorectal Cancer: From Mechanisms to Targeted Therapy Approaches.

Runkai Zhou, Fazhi Wang, Jiazhe Wen, Xuefeng Zhou, Yugang Wen

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 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. The role of NADFrontiers in oncology · 2026
    Review
  5. Article
  6. 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

5 authors.

Runkai ZhouDepartment of General Surgery, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID https://orcid.org/0009-0004-5985-047X
Fazhi WangDepartment of General Surgery, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Jiazhe WenSchool of Basic Medical Sciences, Fudan University, Shanghai, China.
Xuefeng ZhouDepartment of Oncology, The Dongtai Hospital of Nantong University, Dongtai, Jiangsu, China.
Yugang WenDepartment of General Surgery, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

Funding

National Natural Science Foundation of China 81972215
6 · The paper itself

Abstract

backgroundColorectal cancer (CRC) is one of the most common malignant tumors, and its morbidity ranks third among all cancers, with a trend toward younger patients. Metabolic reprogramming, a unique metabolic mode in tumor cells, is closely related to the occurrence and development of CRC. Numerous studies have confirmed that many genetic and protein changes can regulate cellular metabolic reprogramming, of which changes in glucose metabolism have the greatest impact. These aberrant metabolic processes provide energy and essential nutrients to CRC cells, promoting their proliferation and metastasis and influencing tumor resistance. The purpose of this review is to outline the role of glucose metabolic reprogramming in the onset and development of CRC, discuss the research progress in the dual reprogramming of glucose metabolism and lipid metabolism or glucose metabolism and amino acid metabolism, and address the issues of targeted metabolism therapy and drug resistance.

methodsWe searched PubMed for review articles published in English between January 1, 2015, and April 26, 2024, which included "Colorectal Neoplasms" with "Metabolic Reprogramming" OR "Glucose Metabolism Disorders" OR "The Warburg Effect" OR "Targeted Therapy." Subsequently, the literature was classified, organized, and summarized. Various types of studies were integrated and compiled into this review. Additionally, mechanism diagrams were drawn to facilitate the understanding of this study. The figures were created using BioRender.com and has obtained the official publication license.

conclusionsGlucose metabolic reprogramming serves as a pivotal driver of CRC initiation, progression, and chemoresistance, while its crosstalk with lipid or amino acid metabolic reprogramming further amplifies the malignant phenotype of CRC. Targeted therapeutic strategies aiming at glucose metabolic reprogramming (such as metabolic inhibitors, combination with immunotherapy) and related clinical research have demonstrated potential for inhibiting CRC progression and improving treatment outcomes.

Indexed as

Colorectal NeoplasmsGlucoseAnimalsCellular ReprogrammingDrug Resistance, NeoplasmHumansLipid MetabolismMetabolic ReprogrammingMolecular Targeted TherapyWarburg Effect, OncologicGlucosecolorectal cancerglucose metabolismmetabolic reprogrammingtargeted therapy

Identifiers

PMID40884151
PMCPMC12397687

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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.