Evidence map›Paper›PMID 40099624›Full record

ArticleMolecular carcinogenesis2025

CtBP2 Regulates Wnt Signal Through EGR1 to Influence the Proliferation and Apoptosis of DLBCL Cells.

Jianfang Dong, Lihua Li, Xuefei Zhang, Xijing Yin, Zucong Chen

Abstract read
In one paragraph

Article in Molecular carcinogenesis, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

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2citing papers in PubMed
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1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Jianfang DongDepartment of Hematology, The People's Hospital of Dehong, Dehong Hospital Affiliated of Kunming Medical University, Dehong, Yunnan Province, China.
Lihua LiDepartment of Hematology, The People's Hospital of Dehong, Dehong Hospital Affiliated of Kunming Medical University, Dehong, Yunnan Province, China.
Xuefei ZhangDepartment of Hematology, The People's Hospital of Dehong, Dehong Hospital Affiliated of Kunming Medical University, Dehong, Yunnan Province, China.
Xijing YinDepartment of Hematology, The People's Hospital of Dehong, Dehong Hospital Affiliated of Kunming Medical University, Dehong, Yunnan Province, China.
Zucong ChenDepartment of Hematology, The People's Hospital of Dehong, Dehong Hospital Affiliated of Kunming Medical University, Dehong, Yunnan Province, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diffuse large B-cell lymphoma (DLBCL) is the most prevalent form of lymphoma. The overexpression of CtBP2 in tissues may contribute to tumor occurrence and progression. The expression of EGR1 in DLBCL is elevated, suggesting its potential role as an oncogene that promotes the proliferation of DLBCL cells. Database predictions indicate that CtBP2 can bind to EGR1. The objective of the present study was to investigate whether CtBP2 can influence the proliferation and apoptosis of DLBCL cells by regulating the Wnt signaling pathway through EGR1. Western blot assay showed that CtBP2 expression was upregulated in DLBCL cells. Cell proliferation level was detected by CCK8 assay and EdU staining, and the apoptosis level and cycle distribution were analyzed through flow cytometry. Our data indicated that interference with CtBP2 and EGR1 can inhibit the proliferation and cell cycle progression of DLBCL cells while promoting apoptosis. The predictions from the HDOCK server, along with the results of Co-IP experiments, suggested that EGR1 and CtBP2 can effectively bind to each other, with EGR1 positioned downstream of CtBP2 and regulated by it. Furthermore, interference with CtBP2 could also inhibit the expression of the Wnt/β-catenin signaling pathway. Overexpression of EGR1 counteracted the effects of siRNA-CtBP2, promoting cell proliferation and cycle, inhibiting apoptosis and upregulating the expression of the Wnt/β-catenin signaling pathway. From the above experiments, we found that CtBP2 can regulate the Wnt/β-catenin signaling pathway through EGR1 to influence the proliferation and apoptosis of DLBCL cells. Therefore, EGR1 may be one of the key contributors involved in the regulation of Wnt/β-catenin signaling by CtBP2.

Indexed as

Alcohol OxidoreductasesCo-Repressor ProteinsEarly Growth Response Protein 1Lymphoma, Large B-Cell, DiffuseWnt Signaling PathwayApoptosisCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticHumansAlcohol OxidoreductasesCo-Repressor ProteinsCTBP2 protein, humanEarly Growth Response Protein 1EGR1 protein, humanCtBP2DLBCLEGR1Wnt/β‐catenin

Identifiers

PMID40099624
PMCPMC12074560

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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.