Evidence map›Paper›PMID 40937457›Full record

ArticleWorld journal of gastroenterology2025

B cell CLL/lymphoma 10 promotes colorectal cancer cell proliferation and regulates cuproptosis sensitivity through the NF-κB signaling pathway.

Peng-Tuo Xiao, Chang-Feng Li, Yuan-Da Liu, Jing Zhong, Xi-Lun Cui, Chang Liu, Wei Yang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in World journal of gastroenterology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

7 authors.

Peng-Tuo XiaoDepartment of Endoscopy Center, China-Japan Union Hospital of Jilin University, Changchun 130000, Jilin Province, China.
Chang-Feng LiDepartment of Endoscopy Center, China-Japan Union Hospital of Jilin University, Changchun 130000, Jilin Province, China. cfli@jlu.edu.cn.
Yuan-Da LiuDepartment of Endoscopy Center, China-Japan Union Hospital of Jilin University, Changchun 130000, Jilin Province, China.
Jing ZhongMedical Imaging Center, The Third Affiliated Hospital of Changchun University of Chinese Medicine, Changchun 13000, Jilin Province, China.
Xi-Lun CuiDepartment of Endoscopy Center, China-Japan Union Hospital of Jilin University, Changchun 130000, Jilin Province, China.
Chang LiuDepartment of Endoscopy Center, China-Japan Union Hospital of Jilin University, Changchun 130000, Jilin Province, China.
Wei YangDepartment of Immunology, College of Basic Medical Sciences, Jilin University, Changchun 130000, Jilin Province, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundColorectal cancer (CRC) is a major global health burden. B cell CLL/lymphoma 10 (BCL10), a key component of the caspase recruitment domain protein-BCL10-mucosa-associated lymphoid tissue lymphoma paracaspase complexes, is upregulated in CRC and associated with poor patient prognosis, suggesting its potential role in CRC development and progression. Cuproptosis, a novel form of programmed cell death, has emerged as a promising therapeutic strategy for cancer.

aimTo explore the role of BCL10 in regulating the sensitivity of CRC cells to cuproptosis.

methodsA series of

resultsBCL10 promoted CRC cell proliferation, migration, and invasion, while its knockdown had the opposite effects. BCL10 also influenced the sensitivity of CRC cells to cuproptosis, with BCL10 overexpression enhancing resistance and its knockdown increasing sensitivity. The mechanism involved BCL10 modulating the expression of DLAT, a key protein in the copper-induced cell death pathway, through activation of the nuclear factor kappa-B (NF-κB) signaling pathway.

conclusionBCL10 promotes CRC growth and regulates the sensitivity of CRC cells to cuproptosis by activating the NF-κB signaling pathway and modulating DLAT expression. These findings provide a molecular basis for developing BCL10-targeted therapies for CRC.

Indexed as

B-Cell CLL-Lymphoma 10 ProteinColorectal NeoplasmsCopperNF-kappa BAnimalsApoptosisCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansMiceNeoplasm InvasivenessSignal TransductionXenograft Model Antitumor AssaysB-Cell CLL-Lymphoma 10 ProteinBCL10 protein, humanCopperNF-kappa BB cell CLL/lymphoma 10Cell deathColorectal cancerCuproptosisNuclear factor kappa-B

Identifiers

PMID40937457
PMCPMC12421401

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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.