Evidence map›Paper›PMID 40998798›Full record

ArticleCell death discovery2025

TRIM21 promotes colorectal cancer development through regulating DNA replication by TCF3/MCM2/5 axis.

Xintian Zhang, Han Yao, Yichao Hou, Kun Zhou, Yu Liang, Lidan Hou, Xingming Zhang, Wenfeng Wang, Leilei Du, Mengfei Yao and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

12 authors.

Xintian ZhangShanghai Key Laboratory of Gut Microecology and Associated Major Diseases Research, Digestive Disease Research and Clinical Translation Center, Department of Gastroenterology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, 639 Zhi Zao Ju Road, 200011, Shanghai, China.ORCID http://orcid.org/0000-0002-5991-7919
Han YaoShanghai Key Laboratory of Gut Microecology and Associated Major Diseases Research, Digestive Disease Research and Clinical Translation Center, Department of Gastroenterology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, 639 Zhi Zao Ju Road, 200011, Shanghai, China.
Yichao HouShanghai Key Laboratory of Gut Microecology and Associated Major Diseases Research, Digestive Disease Research and Clinical Translation Center, Department of Gastroenterology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, 639 Zhi Zao Ju Road, 200011, Shanghai, China.
Kun ZhouShanghai Key Laboratory of Gut Microecology and Associated Major Diseases Research, Digestive Disease Research and Clinical Translation Center, Department of Gastroenterology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, 639 Zhi Zao Ju Road, 200011, Shanghai, China.
Yu LiangShanghai Key Laboratory of Gut Microecology and Associated Major Diseases Research, Digestive Disease Research and Clinical Translation Center, Department of Gastroenterology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, 639 Zhi Zao Ju Road, 200011, Shanghai, China.
Lidan HouShanghai Key Laboratory of Gut Microecology and Associated Major Diseases Research, Digestive Disease Research and Clinical Translation Center, Department of Gastroenterology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, 639 Zhi Zao Ju Road, 200011, Shanghai, China.
Xingming ZhangCancer Institute, Fudan University Shanghai Cancer Center, Department of Oncology, Shanghai Medical College, Fudan University, 270 Dongan Road, 200032, Shanghai, China.
Wenfeng WangCancer Institute, Fudan University Shanghai Cancer Center, Department of Oncology, Shanghai Medical College, Fudan University, 270 Dongan Road, 200032, Shanghai, China.
Leilei DuCancer Institute, Fudan University Shanghai Cancer Center, Department of Oncology, Shanghai Medical College, Fudan University, 270 Dongan Road, 200032, Shanghai, China.
Mengfei YaoCancer Institute, Fudan University Shanghai Cancer Center, Department of Oncology, Shanghai Medical College, Fudan University, 270 Dongan Road, 200032, Shanghai, China.
Jianhua WangCancer Institute, Fudan University Shanghai Cancer Center, Department of Oncology, Shanghai Medical College, Fudan University, 270 Dongan Road, 200032, Shanghai, China. jianhuaw2007@qq.com.ORCID http://orcid.org/0000-0003-0016-6505
Xiangjun MengShanghai Key Laboratory of Gut Microecology and Associated Major Diseases Research, Digestive Disease Research and Clinical Translation Center, Department of Gastroenterology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, 639 Zhi Zao Ju Road, 200011, Shanghai, China. meng_xiangjun@yahoo.com.ORCID http://orcid.org/0000-0001-9657-0021

Funding

National Natural Science Foundation of China (National Science Foundation of China) 32071377
6 · The paper itself

Abstract

Disrupting DNA replication has been employed for treating cancers. In the present study, we found that Tripartite motif containing 21 (TRIM21) was highly expressed in colorectal cancer (CRC) and could be valuable for predicting the prognosis of CRC patients. Further study demonstrated that TRIM21 positively regulated the expression of MCM2 and MCM5, DNA replication and proliferation of CRC cells both in vitro and in vivo. In addition, TRIM21 knockdown inhibited both replication initiation and velocity, and increased the chemosensitivity of CRC cells to 5-FU and SN-38. Our study also revealed that DNA replication inhibition following TRIM21 knockdown could not be restored by cell cycle checkpoint kinase inhibitors, but partially by Transcription Factor 3 (TCF3) knockdown. TCF3 directly suppressed MCM2 and MCM5 transcription, inhibiting DNA replication. In summary, TRIM21 could influence tumor development and chemosensitivity to replication inhibitors by regulating DNA replication through the TCF3/MCM2/5 axis, suggesting a promising potential for CRC in the clinic.

Identifiers

PMID40998798
PMCPMC12462522

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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.