Evidence map›Paper›PMID 41723511›Full record

ArticleWorld journal of surgical oncology2026

Milk fat globule-EGF factor 8 enhances the proliferation and migration of thyroid carcinoma cells through epithelial-mesenchymal transition and PI3K/AKT signaling pathway.

Lanning Jia, Yue Han, Zuoyu Chen, Yizeng Wang, Ke Zhao, Xianghui He

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Article in World journal of surgical oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Lanning JiaDepartment of General Surgery, Tianjin Medical University General Hospital, Tianjin, China.
Yue HanDepartment of General Surgery, Tianjin Medical University General Hospital, Tianjin, China.
Zuoyu ChenDepartment of General Surgery, Tianjin Medical University General Hospital, Tianjin, China.
Yizeng WangDepartment of General Surgery, Tianjin Medical University General Hospital, Tianjin, China.
Ke ZhaoDepartment of General Surgery, Tianjin Medical University General Hospital, Tianjin, China.
Xianghui HeDepartment of General Surgery, Tianjin Medical University General Hospital, Tianjin, China. hexh88@tmu.edu.cn.

Funding

Science and technology project of Tianjin Education Commission 2020KJ153Zhao Yicheng Foundation (Incubation Fund) Project ZYYFY2018018
6 · The paper itself

Abstract

backgroundMilk fat globule-EGF factor 8 (MFG-E8) has been found to be involved in the development and progression of several carcinomas. However, the role of MFG-E8 in thyroid carcinoma has not been studied yet. This study aimed to investigate the expression and function of MFG-E8 in thyroid carcinoma (TC).

methodsSingle-cell RNA sequencing, transcriptome sequencing, mass spectrometry, and immunohistochemistry were used to analyze MFG-E8 expression in papillary thyroid carcinoma (PTC). Western blotting and RT-PCR were performed to assess MFG-E8 expression in TC cell lines. Stable MFG-E8 knockdown cell lines were established, and functional assays were conducted to evaluate the effects of MFG-E8 on TC cell proliferation, migration, and invasion. Bioinformatics analysis and Western blotting were employed to explore the potential downstream signaling pathways. The association between MFG-E8 expression and immune cell infiltration in the tumor microenvironment was also analyzed using bioinformatics tools.

resultsMFG-E8 expression was significantly upregulated in PTC tumor tissues. It was closely associated with specific PTC subtypes, with higher expression observed in the tall-cell subtype compared to the classic and follicular subtypes. Knockdown of MFG-E8 significantly inhibited TC cell proliferation, migration, and invasion. Mechanistically, MFG-E8 was found to be associated with the regulation of epithelial-mesenchymal transition (EMT)-related processes and linked to the modulation of the PI3K/AKT signaling pathway in TC cells. Furthermore, MFG-E8 correlated with the formation of an immunosuppressive tumor microenvironment by modulating immune cell infiltration and activating the PI3K/AKT pathway in immune cells.

conclusionsOur findings identify MFG-E8 as a key driver of thyroid carcinoma progression, particularly in aggressive subtypes, and highlight its translational value as a prognostic biomarker and promising therapeutic target by targeting the MFG-E8-PI3K/AKT-EMT axis-providing a new clinical framework for personalized treatment of TC.

Indexed as

Antigens, SurfaceBiomarkers, TumorEpithelial-Mesenchymal TransitionMilk ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktThyroid Cancer, PapillaryThyroid NeoplasmsCell Line, TumorCell MovementCell ProliferationFemaleGene Expression Regulation, NeoplasticHumansNeoplasm InvasivenessSignal TransductionAntigens, SurfaceBiomarkers, TumorMFGE8 protein, humanMilk ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktEpithelial-mesenchymal transitionMilk fat globule-EGF factor 8PI3K/AKTThyroid carcinoma

Identifiers

PMID41723511
PMCPMC13032303

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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.