Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026
[MIS18BP1 regulates epithelial-mesenchymal transition, proliferation, and migration of renal cancer cells via the PI3K/AKT pathway].
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Zhao Baofeng, Tan Xueying, Liang Xuewen, Pan Yuyao, Yuan Jiangshui, Song Weiqing
Аннотация
OBJECTIVES: To explore the regulatory role of MIS18BP1 in epithelial-mesenchymal transition (EMT), proliferation, and migration of renal cancer cells and its molecular mechanism.
METHODS: TCGA and GEO databases were used to analyze the expression patterns of MIS18BP1 in kidney renal clear cell carcinoma (KIRC), and its differential expression between tumor and adjacent tissues was validated by immunohistochemistry. The diagnostic value of MIS18BP1 and its correlation with clinicopathological parameters and immune infiltration were evaluated. Weighted gene co-expression network analysis (WGCNA) was performed to identify MIS18BP1-related gene modules for functional enrichment analysis. In renal cancer cell lines (786-O and ACHN), the effects of lentivirus-mediated MIS18BP1 knockdown on cell proliferation and migration were evaluated using CCK-8, colony formation, Transwell, and wound healing assays. Western blotting was performed to determine the expression levels of EMT-related proteins and PI3K/AKT pathway-related proteins, and rescue experiments were carried out using 740Y-P (a PI3K activator).
RESULTS: MIS18BP1 was significantly overexpressed in KIRC tissues and in 786-O and ACHN cells compared with normal renal epithelial cells (HK-2). MIS18BP1 expression level was positively correlated with TNM stage and pathological grade, and showed good diagnostic performance for KIRC (AUC=0.693-0.885). WGCNA and enrichment analyses indicated that MIS18BP1-related genes were significantly enriched in the PI3K/AKT signaling pathway. In cultured renal cancer cells, MIS18BP1 knockdown significantly inhibited the proliferation, migration, and colony-forming ability of the cells, resulting also in decreased expression of N-cadherin and vimentin, increased expression of E-cadherin, and significantly lowered phosphorylation levels of PI3K and AKT. Treatment with 740Y-P partially reversed the inhibitory effects of MIS18BP1 knockdown on cell proliferation and migration.
CONCLUSIONS: MIS18BP1 is overexpressed in renal cancer and is associated with unfavorable clinical features. High expression of MIS18BP1 enhances proliferation and migration of renal cancer cells possibly by promoting EMT via activating the PI3K/AKT signaling pathway.
METHODS: TCGA and GEO databases were used to analyze the expression patterns of MIS18BP1 in kidney renal clear cell carcinoma (KIRC), and its differential expression between tumor and adjacent tissues was validated by immunohistochemistry. The diagnostic value of MIS18BP1 and its correlation with clinicopathological parameters and immune infiltration were evaluated. Weighted gene co-expression network analysis (WGCNA) was performed to identify MIS18BP1-related gene modules for functional enrichment analysis. In renal cancer cell lines (786-O and ACHN), the effects of lentivirus-mediated MIS18BP1 knockdown on cell proliferation and migration were evaluated using CCK-8, colony formation, Transwell, and wound healing assays. Western blotting was performed to determine the expression levels of EMT-related proteins and PI3K/AKT pathway-related proteins, and rescue experiments were carried out using 740Y-P (a PI3K activator).
RESULTS: MIS18BP1 was significantly overexpressed in KIRC tissues and in 786-O and ACHN cells compared with normal renal epithelial cells (HK-2). MIS18BP1 expression level was positively correlated with TNM stage and pathological grade, and showed good diagnostic performance for KIRC (AUC=0.693-0.885). WGCNA and enrichment analyses indicated that MIS18BP1-related genes were significantly enriched in the PI3K/AKT signaling pathway. In cultured renal cancer cells, MIS18BP1 knockdown significantly inhibited the proliferation, migration, and colony-forming ability of the cells, resulting also in decreased expression of N-cadherin and vimentin, increased expression of E-cadherin, and significantly lowered phosphorylation levels of PI3K and AKT. Treatment with 740Y-P partially reversed the inhibitory effects of MIS18BP1 knockdown on cell proliferation and migration.
CONCLUSIONS: MIS18BP1 is overexpressed in renal cancer and is associated with unfavorable clinical features. High expression of MIS18BP1 enhances proliferation and migration of renal cancer cells possibly by promoting EMT via activating the PI3K/AKT signaling pathway.