Pro-tumorigenic effects of HLA-G in Renal Cell Carcinoma
Renal cell carcinoma (RCC) frequently exhibits high expression of the immunomodulatory molecule HLA-G, which promotes immune tolerance and tumor progression. To define the cell-intrinsic transcriptional programs driven specifically by HLA-G1 neo-expression, we generated RCC7/HLA-G1 cells by lentiviral overexpression and compared them with parental RCC7wt cells that lack endogenous HLA-G. Phenotypically, RCC7/HLA-G1 cells display increased proliferation, enhanced migratory capacity, resistance to apoptosis, and accelerated tumor growth in vivo. The purpose of this bulk RNA-sequencing experiment is to characterize the global transcriptional changes induced by HLA-G1 and to identify signaling pathways, gene networks, and regulatory modules that underlie its pro-tumorigenic activity. By comparing RCC7/HLA-G1 tumors with RCC7wt controls, this dataset enables analysis of oncogenic pathways, immune-associated transcriptional suppression (e.g., IFN-?–responsive chemokines), metabolic reprogramming, extracellular matrix remodeling, and enrichment of stem-cell–associated signatures. Overall, these data define the molecular consequences of HLA-G1 expression in RCC and provide mechanistic insight into how HLA-G contributes to tumor aggressiveness and immune evasion.
Renal cell carcinoma (RCC) frequently exhibits high expression of the immunomodulatory molecule HLA-G, which promotes immune tolerance and tumor progression. To define the cell-intrinsic transcriptional programs driven specifically by HLA-G1 neo-expression, we generated RCC7/HLA-G1 cells by lentiviral overexpression and compared them with parental RCC7wt cells that lack endogenous HLA-G. Phenotypically, RCC7/HLA-G1 cells display increased proliferation, enhanced migratory capacity, resistance to apoptosis, and accelerated tumor growth in vivo. The purpose of this bulk RNA-sequencing experiment is to characterize the global transcriptional changes induced by HLA-G1 and to identify signaling pathways, gene networks, and regulatory modules that underlie its pro-tumorigenic activity. By comparing RCC7/HLA-G1 tumors with RCC7wt controls, this dataset enables analysis of oncogenic pathways, immune-associated transcriptional suppression (e.g., IFN-?–responsive chemokines), metabolic reprogramming, extracellular matrix remodeling, and enrichment of stem-cell–associated signatures. Overall, these data define the molecular consequences of HLA-G1 expression in RCC and provide mechanistic insight into how HLA-G contributes to tumor aggressiveness and immune evasion.
European Bioinformatics Institute