Expression data from MCP-1-treated human kidney cancer CRL-1932 cell line

Microarray analysis revealed MCP-1 treatment altered protein folding processes in RCC CRL1932 cells. In response to MCP-1 treatment, CRL1932 cells and xenograft tumors expressed MCP-1-induced protein (MCPIP) which was reported to cause endoplasmic reticulum (ER) stress-induced apoptosis in human cardiomyocytes. In line with MCPIP induction, the expression of ER stress mediators, such as GRP78, PERK, IRE1α, and PDI, as well as molecules involved in ER stress-induced apoptosis, CHOP, calnexin, and Ero1α, presented in MCP-1 treated RCC cell line and xenograft tumors whereas absent or downregulated in untreated controls. TUNEL assay confirmed apoptosis of MCP-1 treated CRL1932 cells. MCPIP ectopically expressed in HEK293 cell resulted in apoptosis. Meta-analysis showed low level of MCP-1 associated with lower one year-survival rate after nephrectomy in RCC. In this dataset, we include the expression array data from human kidney cancer CRL-1932 cell line with or without the treatment of MCP-1. These data were used to obtain genes upregulated in MCP-1-treated CRL-1932 cells. In total, 4 samples were analyzed. We generated the following pairwise comparisons using Affymetrix Expression Console™ Software (version 1.4): CRL 1932 compared with MCP-1-CRL1932. Genes with a P value < 0.05 and a fold-change ≥1.5 were selected. To identify the potential epigenetic targets of MCP-1, we performed Venn diagram analysis with genes showing either up-regulated by MCP-1 treatment.