The effect of leptin on the genome wide enrichment of cJun in OVCAR8 cells

Studies have shown that leptin activates several signaling pathways and stimulates the expression of numerous downstream genes and that the key transcription factor that exerts this effect might serve as a promising therapeutic target in leptin-driven ovarian cancer. cJun is a widely recognized transcription factor that is located downstream of MAPK signaling pathways, and encodes a nuclear protein that regulates various aspects of cell growth and differentiation. c-Jun is activated by JNK through phosphorylation at Ser63, Ser73, Thr91, and Thr93, and by ERK and p38 via increased gene expression. However, whether c-Jun is involved in leptin-mediated stemness maintenance in ovarian cancer remains mostly unknown. We examined the genome-wide enrichment of c-Jun after leptin treatment in the OVCAR8 cell line. OVCAR8 cells were serum starved overnight and then treated with 100 ng/ml leptin for 24 h. Chromatin immunoprecipitation DNA sequencing (ChlPseq) for cJun and H3K27ac in OVCAR8 cells.