Fig. 8: Summary of EC activation during ccRCC progression.
From: Oncostatin M induces epigenetic reprogramming in renal cell carcinoma-associated endothelial cells
Oncostatin M (OSM), secreted by VHL-deficient tubule cells, induces epigenetic changes in ccRCC-associated endothelial cells (ECs) specifically through histone 3 lysine 14 acetylation (K14ac) mediated by histone acetyltransferase 6B (KAT6B). The hyperacetylation facilitates chromatin opening, activating transcription of specific gene sets involved in hypoxic response, vascular remodeling, inflammatory response, and mesenchymal transition, thereby promoting tumor growth and metastasis. Inhibiting OSM or histone acetyltransferase activity could mitigate these pathological EC phenotypes and reduce tumor growth and metastasis.
