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

GSE277884 Homo sapiens Genome binding/occupancy profiling by high throughput sequencing 8 samples Submitted 2025/10/01 Platform GPL24676
Summary
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.
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Also filed as BioProject PRJNA1164701 and SRA study SRP534409. Searching any of these in the dataset finder brings you back here.

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