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JUP drives a PDGFB-JAK-STAT signaling axis to promote ovarian cancer progression

GSE337668 Homo sapiens Expression profiling by high throughput sequencing 6 samples Submitted 2026/07/06 Platform GPL29480
Summary
The Janus kinase (JAK) signaling pathway is frequently associated with ovarian cancer (OC) progression. However, inhibition of JAK signaling has achieved limited therapeutic effects in OC patients, highlighting the need to elucidate the mechanisms underlying JAK dysregulation in OC development. Here, we demonstrate that Junction plakoglobin (JUP) acts as a positive regulator in the JAK signaling pathway in OC. Clinically, JUP expression is significantly upregulated and correlates with poor prognosis in OC patients. Phenotypically, depletion of JUP suppresses OC cell proliferation and migration, whereas overexpression of JUP yielded opposite effects. Mechanistically, JUP drives a PDGFB-JAK-STAT signaling axis through interaction with GABPA. Collectively, our findings establish an oncogenic role of JUP in OC progression via upregulation of JAK signaling and suggest that JUP represents a potential therapeutic target in JAK-driven OC.
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Also filed as BioProject PRJNA1490569 and SRA study SRP715564. Searching any of these in the dataset finder brings you back here.

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