Evidence map›Paper›PMID 41928618›Full record

ArticleHead & neck2026

CCL26-Mediated Modulation of Endothelial Secretome by Hypoxia-Induced Tumor-Derived Exosomes Enhances Metastatic Progression in Head and Neck Cancer.

Ozel Capik, Sevil Tekman, Betul Gundogdu, Ahsen Kilic, Rumeysa Polat, Omer Aydin, Omer Faruk Karatas

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Head & neck, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

7 authors.

Ozel CapikDepartment of Molecular Biology and Genetics, Erzurum Technical University, Erzurum, Turkey.ORCID https://orcid.org/0000-0003-2827-2537
Sevil TekmanDepartment of Molecular Biology and Genetics, Erzurum Technical University, Erzurum, Turkey.
Betul GundogduDepartment of Medical Pathology, Faculty of Medicine, Ataturk University, Erzurum, Turkey.
Ahsen KilicDepartment of Molecular Biology and Genetics, Erzurum Technical University, Erzurum, Turkey.
Rumeysa PolatDepartment of Biomedical Engineering, Erciyes University, Kayseri, Türkiye.
Omer AydinDepartment of Biomedical Engineering, Erciyes University, Kayseri, Türkiye.
Omer Faruk KaratasDepartment of Molecular Biology and Genetics, Erzurum Technical University, Erzurum, Turkey.ORCID https://orcid.org/0000-0002-0379-2088

Funding

Türkiye Bilimsel ve Teknolojik Araştırma Kurumu 123Z593
6 · The paper itself

Abstract

backgroundTumor cells adapt to hypoxia by releasing hiTDExs enriched with bioactive molecules that modulate endothelial behavior and promote tumor progression. This study aimed to characterize how hypoxia-induced HNSCC exosomes reshape the endothelial secretome and contribute to metastatic potential.

methodsWe examined whether hiTDExs reprogram endothelial cells and alter their secretome using cytokine arrays. Functional assays (migration, invasion, tube formation) showed a tumor-promoting role of CCL26 and tumor-suppressive effects of genetic inhibition of its receptor CCR3, while in silico and immunohistochemistry analyses assessed CCL26, HIF1A, and CD31 expression in relation to metastasis.

resultsHypoxic exosomes from Detroit-562 and FaDu cells altered 25 and 52 proteins in HUVEC secretomes, with elevated CCL26 confirmed by ELISA. CCL26 significantly enhanced HNSCC cell proliferation, migration, and invasion, whereas CCL26 neutralization or genetic inhibition of its receptor CCR3 effectively abrogated these effects. High CCL26 and HIF1A correlated with metastasis, advanced stage, and poor survival.

conclusionhiTDExs reprogram endothelial secretomes by elevating CCL26, promoting tumor-supportive phenotypes and driving metastatic progression in HNSCC.

Indexed as

Carcinoma, Squamous CellChemokine CCL26ExosomesHead and Neck NeoplasmsSecretomeCell Line, TumorCell MovementCell ProliferationDisease ProgressionEndothelial CellsFemaleHumansHypoxia-Inducible Factor 1, alpha SubunitMaleNeoplasm InvasivenessNeoplasm MetastasisCCL26 protein, humanChemokine CCL26HIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitCCL26chemokineexosomeshead and neck carcinomahypoxiasecretometumor microenvironment

Identifiers

PMID41928618
PMCPMC13431832

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.