Hematology (Amsterdam, Netherlands) · 2026
VGLL4 regulates the Wnt/β-catenin signaling pathway and acts as an oncogenic factor in acute myeloid leukemia.
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Zhou Chen, Yin Yujin, Gu Juan, Shen He, Yuan Yuchu, Wang Mingyan
Аннотация
OBJECTIVE: To investigate the expression, function, and underlying mechanism of VGLL4 in AML.
METHODS: Bioinformatic analysis of TCGA data by GEPIA website was performed. VGLL4 protein expression was analyzed by Western blot. We then performed functional assays (CCK-8, colony formation, and Transwell) to evaluate the effects of VGLL4 knockdown and overexpression on the proliferation, migration, and Matrigel matrix penetration ability of AML cell lines. Apoptosis was assessed by flow cytometry, and the expression of key Wnt/β-catenin pathway proteins was examined by Western blot.
RESULTS: Compared with controls, VGLL4 was significantly upregulated in AML. Functionally, VGLL4 knockdown potently suppressed AML cell proliferation, migration, and Matrigel matrix penetration ability, promoted apoptosis, and downregulated the expression of key pathway proteins, including β-catenin and GSK3β.
CONCLUSION: VGLL4 acts as an oncogenic factor in AML, potentially through activating the Wnt/β-catenin pathway. Thus, we propose VGLL4 as a promising molecular target for AML therapy.
METHODS: Bioinformatic analysis of TCGA data by GEPIA website was performed. VGLL4 protein expression was analyzed by Western blot. We then performed functional assays (CCK-8, colony formation, and Transwell) to evaluate the effects of VGLL4 knockdown and overexpression on the proliferation, migration, and Matrigel matrix penetration ability of AML cell lines. Apoptosis was assessed by flow cytometry, and the expression of key Wnt/β-catenin pathway proteins was examined by Western blot.
RESULTS: Compared with controls, VGLL4 was significantly upregulated in AML. Functionally, VGLL4 knockdown potently suppressed AML cell proliferation, migration, and Matrigel matrix penetration ability, promoted apoptosis, and downregulated the expression of key pathway proteins, including β-catenin and GSK3β.
CONCLUSION: VGLL4 acts as an oncogenic factor in AML, potentially through activating the Wnt/β-catenin pathway. Thus, we propose VGLL4 as a promising molecular target for AML therapy.