Evidence map›Paper›PMID 41569405›Full record

ArticleJournal of endocrinological investigation2026

Organoid modeling identifies EDN1 as a potential oncogenic driver in papillary thyroid carcinoma via modulation of the Hippo-YAP signaling pathway.

Rui Hai, Fei Wu, Singkome Tima, Chao Li, Yang Zhou, Jie Yao, Songyot Anuchapreeda, Xiangyu Zhou

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of endocrinological investigation, 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

8 authors.

Rui Hai *Department of Medical Technology, Faculty of Associated Medical Sciences, Chiang Mai University, Chiang Mai, 50200, Thailand.
Fei Wu *Department of General Surgery (Thyroid Surgery), the Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China.
Singkome TimaDepartment of Medical Technology, Faculty of Associated Medical Sciences, Chiang Mai University, Chiang Mai, 50200, Thailand.
Chao LiDepartment of Head and Neck Surgery, Sichuan Clinical Research Center for Cancer, Sichuan Cancer Hospital & Institute, Sichuan Cancer Center, Affiliated Cancer Hospital of University of Electronic Science and Technology of China, Chengdu, 610000, China.
Yang ZhouDepartment of Vascular Surgery, Deyang People's Hospital, Deyang, 618000, China.
Jie YaoDepartment of General Surgery (Thyroid Surgery), the Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China.
Songyot AnuchapreedaDepartment of Medical Technology, Faculty of Associated Medical Sciences, Chiang Mai University, Chiang Mai, 50200, Thailand. songyot.anuch@cmu.ac.th.
Xiangyu ZhouDepartment of General Surgery (Thyroid Surgery), the Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China. xiangyuzhou971@vip.126.com.

Funding

Luzhou Municipal People's Government Southwest Medical University Science and Technology Strategic Cooperation Project 2024LZXNYDJ010Southwest Medical University Integrated Traditional Chinese and Western Medicine Special Projectine 2023ZYYQ17
6 · The paper itself

Abstract

backgroundThyroid carcinoma (TC), particularly papillary thyroid carcinoma (PTC), is the most prevalent endocrine malignancy globally. Endothelin-1 (EDN1) has been implicated in tumor progression in various cancers, but its biological role in PTC remains unclear. This study aimed to investigate the expression and function of EDN1 in PTC.

methodsEDN1 expression in PTC cells and tissues was assessed using RT-qPCR and immunofluorescence. Lentiviral knockdown of EDN1 was performed in PTC cells and organoids. Cell proliferation and migration were evaluated via CCK-8, colony formation, and Transwell assays. The effects of EDN1 inhibition were further examined in PTC organoid and murine xenograft models. Western blotting (WB) and immunofluorescence were used to analyze the expression of proliferation-related (PCNA), migration-related (MMP2), and Hippo-YAP signaling proteins.

resultsEDN1 was highly expressed in PTC cells and tissues. Its knockdown significantly suppressed PTC cell proliferation, migration, and tumor growth in xenografts. Additionally, EDN1 deficiency reduced organoid formation efficiency and size. Mechanistically, EDN1 exerted its oncogenic effects partly through the Hippo-YAP pathway.

conclusionOur research findings suggest that EDN1, at least partially through the Hippo-YAP signaling pathway, may exist as a potential oncogenic driver in PTC, suggesting its potential as a diagnostic and therapeutic biomarker for PTC.

Indexed as

Endothelin-1OrganoidsThyroid Cancer, PapillaryThyroid NeoplasmsTranscription FactorsAnimalsCell Line, TumorCell MovementCell ProliferationFemaleGene Expression Regulation, NeoplasticHippo Signaling PathwayHumansMiceMice, NudeSignal TransductionEndothelin-1Transcription FactorsYAP1 protein, humanYAP-Signaling ProteinsEDN1OrganoidPapillary thyroid carcinomaYAP

Identifiers

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.