Tissue & cell · 2026
Exosomal TGFBI promotes malignant progression of melanoma by regulating the FN1 signaling pathway.
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Ge Yongliang, Qiao Jingya, Ju Lingling, Chen Lin, Gao Songnian
Аннотация
OBJECTIVE: This study aimed to investigate the role and mechanism of exosomal Transforming Growth Factor Beta-Induced Protein (TGFBI) in the malignant progression of melanoma.
METHODS: Bioinformatics analyses of the GSE84683 and TCGA-SKCM datasets were performed. Exosomes were isolated from melanoma cell lines and characterized. A series of in vitro functional assays (CCK-8, wound healing, Transwell, tube formation) and in vivo xenograft models were used. Protein interaction was predicted by the STRING database and verified by co-immunoprecipitation (Co-IP). Rescue experiments were conducted to confirm the functional relationship.
RESULTS: TGFBI was significantly overexpressed in melanoma. TGFBI was enriched in melanoma-derived exosomes and could be delivered to recipient cells. Exosomal TGFBI promoted melanoma cell proliferation, migration, invasion, angiogenesis, and tumor growth in vivo. TGFBI was found to physically interact with Fibronectin 1 (FN1). FN1 overexpression reversed the suppressive effects of TGFBI knockdown on melanoma progression.
CONCLUSION: Exosomal TGFBI promotes the malignant progression of melanoma by interacting with and regulating FN1, revealing a potential therapeutic target for this disease.
METHODS: Bioinformatics analyses of the GSE84683 and TCGA-SKCM datasets were performed. Exosomes were isolated from melanoma cell lines and characterized. A series of in vitro functional assays (CCK-8, wound healing, Transwell, tube formation) and in vivo xenograft models were used. Protein interaction was predicted by the STRING database and verified by co-immunoprecipitation (Co-IP). Rescue experiments were conducted to confirm the functional relationship.
RESULTS: TGFBI was significantly overexpressed in melanoma. TGFBI was enriched in melanoma-derived exosomes and could be delivered to recipient cells. Exosomal TGFBI promoted melanoma cell proliferation, migration, invasion, angiogenesis, and tumor growth in vivo. TGFBI was found to physically interact with Fibronectin 1 (FN1). FN1 overexpression reversed the suppressive effects of TGFBI knockdown on melanoma progression.
CONCLUSION: Exosomal TGFBI promotes the malignant progression of melanoma by interacting with and regulating FN1, revealing a potential therapeutic target for this disease.