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MFAP2 promotes epithelial–mesenchymal transition (EMT) through the EGFR-AKT-STAT3 signaling pathway in colorectal cancer (CRC) cells. (A, B) The top 20 enrichment signaling pathways regulated by MFAP2 knockdown. (C, D) VEGFR2 signaling pathway was enriched in the MFAP2 knockdown cells, shown by Gene Set Enrichment Analysis (GSEA) and essential genes in this enrichment. (E) MFAP2 knockdown affected the EGFR-AKT-STAT3 axis.

Journal: Genes & Diseases

Article Title: MFAP2 promotes metastasis and drug resistance by regulating epithelial-to-mesenchymal transition through EGFR signaling pathway in colorectal cancer cells

doi: 10.1016/j.gendis.2025.101800

Figure Lengend Snippet: MFAP2 promotes epithelial–mesenchymal transition (EMT) through the EGFR-AKT-STAT3 signaling pathway in colorectal cancer (CRC) cells. (A, B) The top 20 enrichment signaling pathways regulated by MFAP2 knockdown. (C, D) VEGFR2 signaling pathway was enriched in the MFAP2 knockdown cells, shown by Gene Set Enrichment Analysis (GSEA) and essential genes in this enrichment. (E) MFAP2 knockdown affected the EGFR-AKT-STAT3 axis.

Article Snippet: Following blocking with 5% non-fat milk in PBS with 0.02% Tween 20 detergent (PBST) at room temperature for 2 h, the membranes were incubated with primary antibodies, including MFAP2 (Solarbio, China), GAPDH (BBI Co., Ltd., China), epidermal growth factor receptor (EGFR; Proteintech, China), protein kinase B (AKT) (Proteintech), signal transducer and activator of transcription 3 (STAT3) (Proteintech), and vascular endothelial growth factor A (VEGFA) (Proteintech), p-EGFR (Cell Signaling Technology, USA), p-STAT3 (Cell Signaling Technology), and p-AKT ser473 (Cell Signaling Technology) antibodies, at 4 °C overnight.

Techniques: Protein-Protein interactions, Knockdown