Evidence map›Paper›PMID 40591048›Full record

ArticleCell biology and toxicology2025

KMT2D/ZNF460-induced COL9A1-mediated extracellular matrix stiffness maintains the cancer stem cell pool to promote colorectal cancer progression.

Chengxin Song, Jingmin Xue, Wenjie Song, Xinyu Yue, Yixiu Xia, Peng Han

Abstract read
In one paragraph

Article in Cell biology and toxicology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

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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

3 citing papers in PubMed.

  1. Article
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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

6 authors.

Chengxin SongDepartment of Colorectal Surgery, Harbin Medical University Affiliated Cancer Hospital, No. 150, Haping Road, Nangang District, Harbin, 150081, Heilongjiang, People's Republic of China.
Jingmin XueDepartment of Colorectal Surgery, Harbin Medical University Affiliated Cancer Hospital, No. 150, Haping Road, Nangang District, Harbin, 150081, Heilongjiang, People's Republic of China.
Wenjie SongDepartment of Colorectal Surgery, Harbin Medical University Affiliated Cancer Hospital, No. 150, Haping Road, Nangang District, Harbin, 150081, Heilongjiang, People's Republic of China.
Xinyu YueDepartment of Colorectal Surgery, Harbin Medical University Affiliated Cancer Hospital, No. 150, Haping Road, Nangang District, Harbin, 150081, Heilongjiang, People's Republic of China.
Yixiu XiaDepartment of Colorectal Surgery, Harbin Medical University Affiliated Cancer Hospital, No. 150, Haping Road, Nangang District, Harbin, 150081, Heilongjiang, People's Republic of China.
Peng HanDepartment of Colorectal Surgery, Harbin Medical University Affiliated Cancer Hospital, No. 150, Haping Road, Nangang District, Harbin, 150081, Heilongjiang, People's Republic of China. leospiv@hrbmu.edu.cn.

Funding

Climbing Advantage Discipline Plan of Harbin Medical University Affiliated Cancer Hospital PDYS-2024-14Collaborative Innovation Cultivation Project for Universities in Heilongjiang Province LJGXCG2023-087
6 · The paper itself

Abstract

Collagen is a central component of the extracellular matrix (ECM) in tissues, and ECM can promote tumor cell immune evasion. Our research aimed to expound the biological function of the collagen alpha-1(IX) chain (COL9A1) in colorectal cancer (CRC) and the upstream mechanism regarding KMT2D/ZNF460. COL9A1 contributed to maintaining colorectal cancer stem cells (CCSC) self-renewal and proliferative capacity, and COL9A1 knockdown attenuated CCSC stemness, which was activated by 20.0 kPa polyacrylamide gels. Silencing of COL9A1 hampered tumor growth and stemness in mice induced by AOM/DSS and improved the tumor microenvironment (TME) in xenograft-bearing mice. Mechanistically, KMT2D promoted COL9A1 expression by mediating H3K4me1 modification of the enhancer and recruiting ZNF460. In the presence of attenuated KMT2D signaling, its effect on CCSC stemness and CRC progression was similar to that of knockdown of COL9A1, both of which have therapeutic benefits for CRC tumors. Again, the reactivation of COL9A1 reversed this trend. In conclusion, KMT2D mediates H3K4me1 modification of enhancers and recruits ZNF460 to activate COL9A1, which enhances ECM stiffness and self-renewal of CCSC to remodel TME, contributing to CRC progression.

Indexed as

Colorectal NeoplasmsDNA-Binding ProteinsExtracellular MatrixNeoplastic Stem CellsTranscription FactorsAnimalsCell Line, TumorCell ProliferationDisease ProgressionGene Expression Regulation, NeoplasticHumansMiceMice, Inbred BALB CMice, NudeNeoplasm ProteinsTumor MicroenvironmentDNA-Binding ProteinsKMT2D protein, humanNeoplasm ProteinsTranscription FactorsCOL9A1Colorectal cancerExtracellular matrixKMT2DZNF460

Identifiers

PMID40591048
PMCPMC12213864

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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.