Evidence map›Paper›PMID 39652176›Full record

ArticleNaunyn-Schmiedeberg's archives of pharmacology2025

Treatment of cancer-associated fibroblast-like cells with celecoxib enhances the anti-cancer T helper 1/Treg responses in breast cancer.

Arash Samoudi, Firoozeh Abolhasani-Zadeh, Ali Afgar, Elnaz Jalilian, Hamid Zeinalynezhad, Ladan Langroudi

Abstract read
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In one paragraph

Article in Naunyn-Schmiedeberg's archives of pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Review
  2. Review
  3. Celecoxib in oncology: targeting the COX-2/PGEFrontiers in pharmacology · 2025
    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

6 authors.

Arash SamoudiDepartment of Medical Immunology, School of Medicine, Kerman University of Medical Sciences, Pajoohesh Sq, Kerman, 7616914111, Iran.
Firoozeh Abolhasani-ZadehDepartment of Surgery, School of Medicine, Kerman University of Medical Sciences, Kerman, Iran.
Ali AfgarResearch center for Hydatid Disease in Iran, Kerman University of Medical Sciences, Kerman, Iran.
Elnaz JalilianDepartment of Medical Immunology, School of Medicine, Kerman University of Medical Sciences, Pajoohesh Sq, Kerman, 7616914111, Iran.
Hamid ZeinalynezhadDepartment of Surgery, School of Medicine, Kerman University of Medical Sciences, Kerman, Iran.
Ladan LangroudiDepartment of Medical Immunology, School of Medicine, Kerman University of Medical Sciences, Pajoohesh Sq, Kerman, 7616914111, Iran. l.langroudi@kmu.ac.ir.

Funding

Kerman univ IR.KMU.REC.1398.257
6 · The paper itself

Abstract

Tumor inflammation, as one of the hallmarks of cancer, has been the target for anti-cancer treatments. Celecoxib is a selective inhibitor of the enzyme cycloxygenase-2 (COX-2) and inhibits the production of PGE2, which is an important mediator of tumor inflammation produced by cancer cells and cells of the tumor microenvironment. In this study, we aimed at inhibiting COX-2 using celecoxib, expressed in cancer-associated fibroblast (CAF)-like cells isolated from breast cancer and evaluated the alterations in their cytokine profile and gene expression. CAF-like cells were isolated by explant culture from 13 breast cancer tissues. Simultaneously, peripheral blood mononuclear cells (PBMCs) were isolated from patients' blood. CAF-like cells were treated with 10 µM of celecoxib and expression of genes COX-2, smooth muscle actin-alpha (α-SMA), and production of prostaglandin E2 (PGE2), Interleukin 10 (IL10), and transforming growth factor beta1 (TGF-β1) was evaluated. Next, PBMCs were co-cultured with celecoxib-treated CAF-like cells and the expression of genes T-bet, Foxp3, GATA-3; production of cytokines IFN-ɣ, IL-10, IL-4, TGF-β1, and the mediator PGE2 were assessed by real-time-PCR and ELISA, respectively. Isolated CAF-like cells showed expression of fibroblast activation protein (FAP). Treatment with celecoxib was able to efficiently reduce the production of PGE2 and the expression of α-SMA in isolated CAF-like cells. Furthermore, PBMCs in co-culture with these cells showed enhanced Th1 phenotype including T-bet and IFNγ expression and decreased the phenotypical markers of regulatory T cells such as FoxP3 and IL-10 and TGF-β1 production. Our study shows the important role of COX-2 in CAFs by promoting immune suppression. Our results suggested that high expression of COX-2 in CAFs may serve as a new therapeutic, targeting CAFs in enhancing immune responses in breast cancer treatment.

Indexed as

Antineoplastic AgentsBreast NeoplasmsCancer-Associated FibroblastsCelecoxibCyclooxygenase 2 InhibitorsTh1 CellsT-Lymphocytes, RegulatoryCoculture TechniquesCyclooxygenase 2CytokinesDinoprostoneFemaleHumansMiddle AgedTumor MicroenvironmentAntineoplastic AgentsCelecoxibCyclooxygenase 2Cyclooxygenase 2 InhibitorsCytokinesDinoprostonePTGS2 protein, humanCancer-associated fibroblastsCelecoxibCycloxygenase-2ImmunotherapyTumor microenvironment

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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.