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Background <p>Milk 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).</p> Methods <p>Single-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.</p> Results <p>MFG-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.</p> Conclusions <p>Our 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.</p>

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

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年2月21日

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

摘要

Background

Milk 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).

Methods

Single-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.

Results

MFG-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.

Conclusions

Our 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.