Evidence map›Paper›PMID 38816600›Full record

ArticleDigestive diseases and sciences2024

KLF4 Induces Colorectal Cancer by Promoting EMT via STAT3 Activation.

Lebin Yuan, Yanqiu Meng, Jiajia Xiang

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Article in Digestive diseases and sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

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0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

Who cites it

7 citing papers in PubMed.

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4 · The record

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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

3 authors.

Lebin Yuan *Department of Nail and Breast Surgery, Affiliated Xiangyang Central Hospital of Hubei University of Arts and Science, Xiangyang Center Hospital, Xiangyang, Hubei, China.
Yanqiu Meng *Oncology Department, First Affiliated Hospital of Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, China.
Jiajia XiangMolecular Centre Laboratory, The Second Affiliated Hospital of Nanchang University, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, China. ndefy21226@ncu.edu.cn.

Funding

5511 Science and Technology Innovation Talent Project of Jiangxi Province GJJ2200241
6 · The paper itself

Abstract

objectiveKrüppel-like factor 4 (KLF4) has been demonstrated to exert a pro-carcinogenic effect in solid tissues. However, the precise biological function and underlying mechanisms in colorectal cancer (CRC) remains elucidated.

aimsTo investigate whether KLF4 participates in the proliferation and invasion of CRC.

methodsThe expression of KLF4 was investigated using immunohistochemistry and immunoblotting. The clinical significance of KLF4 was evaluated. Furthermore, the effect of inhibiting or overexpressing KLF4 on tumor was examined. Immunoblotting and qPCR were used to detect Epithelial-mesenchymal transition-related proteins levels. Additionally, the molecular function of KLF4 is related to the STAT3 signaling pathway and was determined through JASPAR, GSEA analysis, and in vitro experiments.

resultsKLF4 exhibits down-regulated expression in CRC and is part of the vessel invasion, TNM stage, and worse prognosis. In vitro studies have shown that KLF4 promotes cellular proliferation and invasion, as well as EMT processes. Xenograft tumor models confirmed the oncogenic role of KLF4 in nude mice. Furthermore, GSEA and JASPAR databases analysis reveal that the binding of KLF4 to the signal transducer and activator of transcription 3 (STAT3) promoter site induces activation of p-STAT3 signaling. Subsequent targeting of STAT3 confirmed its pivotal role in mediating the oncogenic effects exerted by KLF4.

conclusionThe study suggests that KLF4 activates STAT3 signaling, inducing epithelial-mesenchymal transition, thereby promoting CRC progression.

Indexed as

Cell ProliferationColorectal NeoplasmsEpithelial-Mesenchymal TransitionKruppel-Like Factor 4Kruppel-Like Transcription FactorsMice, NudeSTAT3 Transcription FactorAnimalsCell Line, TumorFemaleGene Expression Regulation, NeoplasticHumansMaleMiceMice, Inbred BALB CMiddle AgedKLF4 protein, humanKlf4 protein, mouseKruppel-Like Factor 4Kruppel-Like Transcription FactorsSTAT3 protein, humanSTAT3 Transcription FactorColorectal cancerInvasionKLF3ProliferationSTAT3

Identifiers

PMID38816600

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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.