Evidence map›Paper›PMID 39720975›Full record

ArticleApoptosis : an international journal on programmed cell death2025

TRIM23 promotes 5-Fluorouracil resistance in colorectal cancer by upregulating GALNT4 expression.

Shanshan Wei, Wei Xia, Jun Feng, Jianwen Lu, Luo Zhang, Wei Wang, Wenwei Hu, Yiting Geng

Abstract read
In one paragraph

Article in Apoptosis : an international journal on programmed cell death, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Death never dies: increasing impact of programmed cell death.Apoptosis : an international journal on programmed cell death · 2025
    Article
  2. A cellular danse macabre: the choreography of programmed cell death.Apoptosis : an international journal on programmed cell death · 2025
    Article
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.

Shanshan WeiDepartment of Oncology, The Third Affiliated Hospital of Soochow University, Changzhou, Jiangsu, 213003, China.
Wei XiaDepartment of Oncology, The Third Affiliated Hospital of Soochow University, Changzhou, Jiangsu, 213003, China.
Jun FengDepartment of Oncology, The Third Affiliated Hospital of Soochow University, Changzhou, Jiangsu, 213003, China.
Jianwen LuDepartment of Oncology, The Third Affiliated Hospital of Soochow University, Changzhou, Jiangsu, 213003, China.
Luo ZhangDepartment of Oncology, The Third Affiliated Hospital of Soochow University, Changzhou, Jiangsu, 213003, China.
Wei WangDepartment of Oncology, The Third Affiliated Hospital of Soochow University, Changzhou, Jiangsu, 213003, China.
Wenwei HuDepartment of Oncology, The Third Affiliated Hospital of Soochow University, Changzhou, Jiangsu, 213003, China. huwenwei@suda.edu.cn.
Yiting GengDepartment of Oncology, The Third Affiliated Hospital of Soochow University, Changzhou, Jiangsu, 213003, China. gyt1986@suda.edu.cn.

Funding

Changzhou "14th Five-Year Plan" High-level Health Personnel Training Project 2022260Jiangsu Province Traditional Chinese Medicine Technology Development Plan Project MS2023086Science and Technology Project of Changzhou Health Commission (Major project) ZD202302
6 · The paper itself

Abstract

5-Fluorouracil (5-FU) is one of the most common chemotherapeutic agents for colorectal cancer (CRC), but its application is often limited by resistance. Tripartite motif containing 23 (TRIM23) has been reported to be dysregulated in various tumors and involved in tumor progression and chemotherapy resistance. However, its relationship with CRC 5-FU resistance and the underlying mechanism are still unclear. In this study, we found that TRIM23 was upregulated in CRC. Patients treated with 5-FU and with high TRIM23 expression had a lower disease control rate (DCR) and a poorer median progression-free survival (mPFS). In vitro, the expression of TRIM23 in CRC cells was elevated after 5-FU treatment. Compared to parental cells, TRIM23 was significantly overexpressed in 5-FU-resistant CRC cells. Mechanistically, TRIM23 mediated 5-FU resistance of CRC by upregulating the expression of N-acetylgalactosaminyltransferase-4 (GALNT4). Knocking down TRIM23 in 5-FU-resistant colon cancer cells restored the sensitivity to 5-FU, while overexpression of GALNT4 in TRIM23 knockdown cells counteracted the chemosensitization caused by TRIM23 downregulation. The TRIM23/GALNT4 axis may play a crucial role in 5-FU resistance in CRC, and targeted inhibition of this axis is expected to reverse resistance. As a potential biomarker for screening 5-FU-sensitive patients and predicting prognosis in clinical practice, TRIM23 deserves further investigation.

Indexed as

Colorectal NeoplasmsDrug Resistance, NeoplasmFluorouracilN-AcetylgalactosaminyltransferasesAnimalsCell Line, TumorFemaleGene Expression Regulation, NeoplasticHumansMaleMiceMiddle AgedPolypeptide N-acetylgalactosaminyltransferaseUp-RegulationFluorouracilN-AcetylgalactosaminyltransferasesPolypeptide N-acetylgalactosaminyltransferase5-FluorouracilColorectal cancerN-acetylgalactosaminyltransferase-4ResistanceTripartite motif containing 23

Identifiers

PMID39720975
PMCPMC11947064

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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.