GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE314nnn/GSE314546/primary200OKTranscriptomicsHomo sapiensExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE314546GEOGSEfalseThe Reciprocal activation between Leptin Receptor and Hippo/YAP axis in Triple Negative Breast Cancer Development [RNA-Seq adipocytes]Triple negative breast cancer (TNBC) is the most aggressive breast cancer subtype with limited effective targets. The over-activation of Hippo/YAP axis is often observed in TNBC, but effective therapeutics inhibitors targeting Hippo pathway are still unavailable in clinics. Recently studies implicated the potential link between obesity and increased breast cancer risk, while the adipocytes in mammary gland played important roles in TNBC development but the detailed mechanism is still unclear. In our study, we identified leptin signaling as an important mediator for Hippo/YAP activation and TNBC progression. The paracrine leptin from adipocytes activated leptin receptor (LEPR), which subsequently induced YAP Tyr357 phosphorylation and YAP nuclear trans-location via LEPR/JAK2/SRC axis. Besides, YAP could also bind to the LEPR promoter and enhance its transcription, thereby forming a positive feedback loop in TNBC progression. The paracrine leptin by adipocytes could activate the positive feedback between leptin signaling and Hippo pathway in TNBC development and progression, while pharmaceutical targeting such loop via LEPR inhibition could significantly suppress TNBC carcinogenesis and progression. In collection, our data identified a novel mechanism by the inter-play between leptin system and Hippo/YAP axis in adipocyte-induced breast cancer development and a promising strategy by targeting the membrane receptor LEPR for TNBC therapy.2026/10/01GSE314546GSM9401462GSM9401466GSM9401465GSM9401464GSM9401463GSM940146724676314546Homo sapiens