Evidence map›Paper›PMID 42776394›Full record

ArticleMolecular biomedicine2026

The DCBLD2 super-enhancer drives colorectal cancer progression through FOSL2/JUND-mediated activation of the CD146/AKT/TNFRSF6B pathway.

Tong Wu, Lan Shao, Xin Hu, Hongjuan He, Lu Chen, Meiqi Feng, Chengjin Qi, Ziwen Wang, Haoran Yu, Boshu Ji and 3 more

Abstract read
In one paragraph

Article in Molecular biomedicine, 2026. 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

13 authors.

Tong WuSchool of Life Science and Technology, Faculty of Life Sciences and Medicine, Harbin Institute of Technology, Harbin, 150001, China.
Lan ShaoDepartment of Medicine, Dalian University of Technology, Dalian, China.
Xin HuSchool of Life Science and Technology, Faculty of Life Sciences and Medicine, Harbin Institute of Technology, Harbin, 150001, China.
Hongjuan HeSchool of Life Science and Technology, Faculty of Life Sciences and Medicine, Harbin Institute of Technology, Harbin, 150001, China.
Lu ChenDepartment of Pathology, the Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Meiqi FengSchool of Life Science and Technology, Faculty of Life Sciences and Medicine, Harbin Institute of Technology, Harbin, 150001, China.
Chengjin QiSchool of Life Science and Technology, Faculty of Life Sciences and Medicine, Harbin Institute of Technology, Harbin, 150001, China.
Ziwen WangSchool of Life Science and Technology, Faculty of Life Sciences and Medicine, Harbin Institute of Technology, Harbin, 150001, China.
Haoran YuDepartment of Biomedical Engineering, School of Medical Information and Engineering, Guangdong Pharmaceutical University, Guangzhou, China.
Boshu JiDepartment of Pathology, the Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Yijia CaoSchool of Life Science and Technology, Faculty of Life Sciences and Medicine, Harbin Institute of Technology, Harbin, 150001, China.
Yan ZhangSchool of Life Science and Technology, Faculty of Life Sciences and Medicine, Harbin Institute of Technology, Harbin, 150001, China. zhangtyo@hit.edu.cn.
Qiong WuSchool of Life Science and Technology, Faculty of Life Sciences and Medicine, Harbin Institute of Technology, Harbin, 150001, China. kigo@hit.edu.cn.

Funding

Key Research and Development Program of heilongjiang 2023ZX06C09National Natural Science Foundation of China 62372141
6 · The paper itself

Abstract

Super-enhancers are clusters of cis-regulatory elements that sustain the expression of cell-identity genes. Their aberrant activation or dysfunction constitutes a hallmark of malignant cellular transformation, which frequently rewires oncogenic transcriptional programs to support uncontrolled cell proliferation and metastatic potential. However, the functions and epigenetic regulation mechanisms of colorectal cancer specific super-enhancers remain poorly understood, and few studies have focused on dissecting how tumor enriched super-enhancers mediate downstream oncogenic signaling in CRC. By integrating multi-omics sequencing data, we identified a highly active super-enhancer in colorectal cancer, termed DCBLD2-SE. Through luciferase reporter assays, the SE3-2 subregion was identified as the minimal functional core of this super-enhancer. Mechanistic studies confirmed that transcription factors of the activator protein-1 family (FOSL2 and JUND) can bind directly to the SE3-2 cis-regulatory element, synergistically regulating local chromatin remodeling and strongly driving the upregulation of the target gene DCBLD2. Following knockout of the DCBLD2-SE core region, the malignant proliferative capacity of colorectal cancer cells decreased significantly, and the growth of xenograft tumors in vivo was markedly inhibited. Functionally, DCBLD2-SE facilitates tumor progression through a DCBLD2-dependent CD146/AKT/TNFRSF6B signaling axis. Clinically, high expression of DCBLD2 correlates with malignant metastasis and poor overall survival in patients with colorectal cancer. In summary, this study uncovers a previously undescribed DCBLD2-centered regulatory cascade that promotes colorectal cancer initiation and progression. DCBLD2-SE and its binding transcription factor activator protein-1 represent promising prognostic biomarkers and actionable therapeutic targets for colorectal cancer.

Indexed as

Colorectal NeoplasmsFos-Related Antigen-2Proto-Oncogene Proteins c-aktProto-Oncogene Proteins c-junSignal TransductionSuper EnhancersAnimalsCell Line, TumorCell ProliferationDisease ProgressionGene Expression Regulation, NeoplasticHumansMiceFOSL2 protein, humanFos-Related Antigen-2JunD protein, humanProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-junActivator protein-1 transcription factorsAKT signaling pathwayColorectal cancerDCBLD2Epigenetic regulationSuper-enhancer

Identifiers

PMID42776394
PMCPMC13601434

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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.