Evidence map›Paper›PMID 41495850›Full record

ArticleEuropean journal of medical research2026

G-CSF promotes H3K27ac-modified KLF5 to activate CXCR4 expression and drive colon cancer growth and metastasis.

Guoqing Ma, Jing Jiang, Tingting He, Canhui Jin, Wenhao Wu, Wufeng Fan, Tianbao Wang, Ping Zhou

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in European journal of medical research, 2026. 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

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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

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

8 authors.

Guoqing MaDepartment of Gastrointestinal Surgery, South China Hospital of Shenzhen University, Shenzhen University, Shenzhen, 518000, Guangdong, China.
Jing JiangDepartment of Gastrointestinal Surgery, South China Hospital of Shenzhen University, Shenzhen University, Shenzhen, 518000, Guangdong, China.
Tingting HeDepartment of Gastrointestinal Surgery, South China Hospital of Shenzhen University, Shenzhen University, Shenzhen, 518000, Guangdong, China.
Canhui JinDepartment of Gastrointestinal Surgery, South China Hospital of Shenzhen University, Shenzhen University, Shenzhen, 518000, Guangdong, China.
Wenhao WuDepartment of Gastrointestinal Surgery, South China Hospital of Shenzhen University, Shenzhen University, Shenzhen, 518000, Guangdong, China.
Wufeng FanDepartment of Gastrointestinal Surgery, South China Hospital of Shenzhen University, Shenzhen University, Shenzhen, 518000, Guangdong, China.
Tianbao WangDepartment of Gastrointestinal Surgery, South China Hospital of Shenzhen University, Shenzhen University, Shenzhen, 518000, Guangdong, China.
Ping ZhouDepartment of Gastrointestinal Surgery, Shenzhen Qianhai Taikang Hospital, No. 3099, Menghai Avenue, Nanshan District, Shenzhen, 518066, Guangdong, China. zpiiisz1@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveThis study investigated how granulocyte colony-stimulating factor (G-CSF) regulates colon cancer (CC) progression through epigenetic activation of the kruppel-like factor 5 (KLF5)/chemokine receptor type 4 (CXCR4) axis.

methodsHuman CC LoVo cells were exposed to G-CSF (20 ng/mL) alone in combination with si-KLF5, oe-CXCR4, or the CXCR4 antagonist AMD3100 for 24 h. Malignant behaviors were evaluated by CCK-8, colony formation, and Transwell assays. H3K27ac modification on the KLF5 promoter and KLF5 binding to the CXCR4 promoter were examined using immunofluorescence, dual-luciferase reporter, and ChIP assays. An orthotopic LoVo xenograft mouse model was used to assess tumor growth, metastasis, and epithelial-mesenchymal transition (EMT) marker expression. KLF5 and CXCR4 mRNA and protein levels were measured in CC cells and tissues via RT-qPCR and western blot.

resultsG-CSF enhanced LoVo cell proliferation, migration, and invasion in a dose-dependent manner, concomitant with increased H3 acetylation and histone H3 lysine 27 (H3K27ac) acetylation. Mechanistically, G-CSF upregulated KLF5 expression via H3K27ac modification, promoting CXCR4 transcriptional activation. Inhibition of KLF5 or CXCR4 partially reversed G-CSF-induced EMT and malignant phenotypes. In vivo, G-CSF accelerated tumor growth and metastasis through the KLF5/CXCR4 signaling pathway, confirming its pro-tumorigenic role.

conclusionsG-CSF drives CC progression by enhancing H3K27ac-dependent upregulation of KLF5, which transactivates CXCR4 to promote EMT, proliferation and metastasis. Targeting the G-CSF/KLF5/CXCR4 axis may represent a potential therapeutic strategy for advanced CC.

Indexed as

Colonic NeoplasmsGranulocyte Colony-Stimulating FactorHistonesKruppel-Like Transcription FactorsReceptors, CXCR4AnimalsCell Line, TumorCell MovementCell ProliferationEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHumansMiceMice, Inbred BALB CMice, NudeNeoplasm MetastasisCXCR4 protein, humanGranulocyte Colony-Stimulating FactorHistonesKLF5 protein, humanKruppel-Like Transcription FactorsReceptors, CXCR4Chemokine receptor type 4Epithelial-mesenchymal transitionGranulocyte colonyHistone 3 lysine 27 acetylationHuman colon cancer LoVo cellsKruppel-like factor 5MetastasisProliferationStimulating factor

Identifiers

PMID41495850
PMCPMC12870162

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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 Socratic graph.