Evidence map›Paper›PMID 38888512›Full record

ArticleAging2024

The crosstalk role of CDKN2A between tumor progression and cuproptosis resistance in colorectal cancer.

Xifu Cheng, Famin Yang, Yuanheng Li, Yuke Cao, Meng Zhang, Jiameng Ji, Yuxiao Bai, Qing Li, Qiongfang Yu, Dian Gao

Abstract read
In one paragraph

Article in Aging, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
–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

20 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
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  5. Article
  6. Review
  7. Harnessing Cuproptosis resistance to advance cancer therapeutics.Apoptosis : an international journal on programmed cell death · 2026
    Review
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  11. Article
  12. Article
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  16. Article
  17. Cancer therapy resistance from a spatial-omics perspective.Clinical and translational medicine · 2025
    Review
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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

10 authors.

Xifu ChengDepartment of Gastroenterology and Hepatology, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang 330006, China.
Famin YangDepartment of Pathogen Biology and Immunology, School of Basic Medical Sciences, Jiangxi Medical College, Nanchang University, Nanchang 330006, China.
Yuanheng LiQueen Mary School, Jiangxi Medical College, Nanchang University, Nanchang 330031, China.
Yuke CaoSchool of Ophthalmology and Optometry, Jiangxi Medical College, Nanchang University, Nanchang 330006, China.
Meng ZhangDepartment of Pathogen Biology and Immunology, School of Basic Medical Sciences, Jiangxi Medical College, Nanchang University, Nanchang 330006, China.
Jiameng JiDepartment of Pathogen Biology and Immunology, School of Basic Medical Sciences, Jiangxi Medical College, Nanchang University, Nanchang 330006, China.
Yuxiao BaiDepartment of Pathogen Biology and Immunology, School of Basic Medical Sciences, Jiangxi Medical College, Nanchang University, Nanchang 330006, China.
Qing LiDepartment of Oncology, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang 330006, China.
Qiongfang YuDepartment of Gastroenterology and Hepatology, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang 330006, China.
Dian GaoDepartment of Pathogen Biology and Immunology, School of Basic Medical Sciences, Jiangxi Medical College, Nanchang University, Nanchang 330006, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCuproptosis is a type of cell death characterized by excessive copper-lipid reactions in the tricarboxylic acid cycle, resulting in protein toxicity stress and cell death. Although known as a cuproptosis inhibitor through CRISPR-Cas9 screening, the role of cyclin-dependent kinase inhibitor 2A (CDKN2A) in cuproptosis resistance and its connection to tumor development remains unclear.

methodsIn this study, we combined single-cell sequencing, spatial transcriptomics, pathological image analysis, TCGA multi-omics analysis and

resultsOur findings showed an increasing trend in cuproptosis in the trajectory of tumor progression, accompanied by an upward trend of CDKN2A. CDKN2A underwent transcriptional activation by MEF2D and via the SNHG7/miR-133b axis, upregulating glycolysis, copper metabolism and copper ion efflux. CDKN2A likely drives epithelial-mesenchymal transition (EMT) and progression by activating Wnt signaling. CDKN2A is associated with high genomic instability and sensitivity to radiation and chemotherapy. Tumor regions expressing CDKN2A exhibit distinctive SPP1+ tumor-associated macrophage (TAM) infiltration and MMP7 enrichment, along with unique signaling crosstalk with adjacent areas.

conclusionsCDKN2A mediates cuproptosis resistance through regulating glycolysis and copper homeostasis, accompanied by a malignant phenotype and pro-tumor niche. Radiation and chemotherapy are expected to potentially serve as therapeutic approaches for cuproptosis-resistant colorectal cancer with high CDKN2A expression.

Indexed as

Colorectal NeoplasmsCyclin-Dependent Kinase Inhibitor p16Disease ProgressionCell Line, TumorCopperDrug Resistance, NeoplasmEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHumansRNA, Long NoncodingCDKN2A protein, humanCopperCyclin-Dependent Kinase Inhibitor p16RNA, Long NoncodingbioinformaticsCDKN2Acuproptosismetabolismradiation therapy

Identifiers

PMID38888512
PMCPMC11236303

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.