Evidence map›Paper›PMID 41408455›Full record

ArticleScientific reports2025

CCL8 suppresses ovarian cancer progression via M1 macrophage polarization and NF-κB-mediated apoptosis.

Jie Fang, Xinyue Zhao, Jin Wang, Yaping Yang, Yujia Xiao

Abstract read
In one paragraph

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

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. Article
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

5 authors.

Jie Fang *Department of Gynecology, The Affiliated Hospital of Jiangsu University, Jiangsu University, Zhenjiang, 212001, Jiangsu, China. fangjie070@163.com.
Xinyue Zhao *Department of Gynecology, The Affiliated Hospital of Jiangsu University, Jiangsu University, Zhenjiang, 212001, Jiangsu, China.
Jin WangDepartment of Gynecology, The Affiliated Hospital of Jiangsu University, Jiangsu University, Zhenjiang, 212001, Jiangsu, China.
Yaping YangDepartment of Gynecology, The Affiliated Hospital of Jiangsu University, Jiangsu University, Zhenjiang, 212001, Jiangsu, China.
Yujia XiaoDepartment of Gynecology, The Affiliated Hospital of Jiangsu University, Jiangsu University, Zhenjiang, 212001, Jiangsu, China.

Funding

the Key Research Foundation of Zhenjiang Social Development SH2023026
6 · The paper itself

Abstract

CCL8, a chemokine overexpressed in ovarian cancer (OC), has drawn attention for its role in tumor progression. This study aimed to explore the function of CCL8 in OC and its effects on tumor-associated macrophages (TAMs) and related mechanisms. Bioinformatics analysis revealed a correlation between high CCL8 expression and M1 macrophage infiltration, as well as a favourable prognosis in OC patients. In vitro, CCL8 polarised THP1-derived macrophages towards an M1 phenotype, and the conditioned medium from these macrophages suppressed ES2 cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT). Mechanistically, CCL8-induced macrophages promoted apoptosis in OC cells via activation of the NF-κB p65 pathway, as evidenced by increased Bax and Caspase3 expression, and these effects were reversed by p65 inhibition. The findings demonstrate that CCL8 exerts a tumor-uppressive effect by inducing M1 macrophage polarisation and activating the NF-κB pathway, positioning it as a potential immunotherapeutic target in OC.

Indexed as

ApoptosisChemokine CCL8MacrophagesNF-kappa BOvarian NeoplasmsTumor-Associated MacrophagesCell Line, TumorCell MovementCell ProliferationDisease ProgressionEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHumansSignal TransductionTranscription Factor RelACCL8 protein, humanChemokine CCL8NF-kappa BRELA protein, humanTranscription Factor RelACCL8MacrophagesNF-κBOvarian cancerP65

Identifiers

PMID41408455
PMCPMC12830605

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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.