Fig. 1: MUC1-C is upregulated in EBVaGC tumor tissues and regulates EBVaGC cell transcriptomes. | Oncogene

Fig. 1: MUC1-C is upregulated in EBVaGC tumor tissues and regulates EBVaGC cell transcriptomes.

From: MUC1-C auto-regulatory complex with EBNA1 is responsible for latent Epstein-Barr virus-associated gastric cancer progression

Fig. 1

A Analysis of the TCGA STAD dataset for MUC1 expression in EBV-positive vs EBV-negative, CIN-negative and MSI-negative GCs. B IHC detection of MUC1-C expression in metastatic EBVaGC tumor tissue and normal gastric epithelium. The bar represents 100 μm. C YCCEL1 cytosolic, membrane and soluble nuclear fractions were immunoblotted with antibodies against the indicated proteins. D Lysates from YCCEL1/tet-CshRNA and YCCEL1/tet-MUC1shRNA cells treated with vehicle or DOX for 7 days were immunoblotted with antibodies against the indicated proteins. E Volcano plot of down- and up-regulated genes in YCCEL1/tet-MUC1shRNA cells treated with vehicle of DOX for 7 days. GSEA of RNA-seq data from YCCEL1 (F) and SNU-719 (G) cells with MUC1-C silencing using the using the HALLMARK E2F TARGETS gene signature. Lysates from YCCEL1/tet-MUC1shRNA (H) and SNU-719/tet-MUC1shRNA (I) cells treated with vehicle of DOX for 7 days were immunoblotted with antibodies against the indicated proteins. J Lysates from YCCEL1/CshRNA and YCCEL1/MUC1shRNA#2 cells were immunoblotted with antibodies against the indicated proteins. K Lysates from YCCEL1 cells treated with 5 μM GO-203 for 4 days were immunoblotted with antibodies against the indicated proteins. L YCCEL1/tet-MUC1shRNA cells were treated with vehicle or DOX for 7 days and analyzed for cell cycle distribution by flow cytometry. The results (mean ± SD of three determinations) are expressed as the percentage of cells in G1, S and G2/M phases.

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