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Updated: Jan 8, 2026

Monitoring Hippo Signaling Pathway Activity Using a Luciferase-based Large Tumor Suppressor LATS Biosensor
Published on: September 13, 2018
PRSS23 promotes pancreatic cancer progression through regulating Hippo-YAP activity
Zhihong Liu1, Qiuping Jiang2, Yuanmeng Sun1
1Central Laboratory, The Affiliated Taizhou People's Hospital of Nanjing Medical University, Taizhou School of Clinical Medicine, Nanjing Medical University, Taizhou, Jiangsu, 225300, China.
PRSS23 is a key driver of pancreatic cancer (PDAC) progression. Inhibiting PRSS23 may offer a new therapeutic strategy for PDAC by disrupting the Hippo signaling pathway and YAP activation.
Area of Science:
- Oncology
- Molecular Biology
- Signaling Pathways
Background:
- Pancreatic ductal adenocarcinoma (PDAC) is an aggressive cancer with poor survival rates.
- Understanding PDAC's molecular drivers is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the role of PRSS23 in PDAC pathogenesis.
- To identify PRSS23's downstream molecular targets and signaling pathways involved in PDAC.
Main Methods:
- Clinical analysis of PRSS23 expression in PDAC tissues.
- In vitro and in vivo functional experiments (knockdown, proliferation, metastasis assays).
- Transcriptomic profiling, molecular docking, and co-immunoprecipitation to elucidate signaling mechanisms.
Main Results:
- PRSS23 is overexpressed in PDAC and linked to reduced patient survival.
- PRSS23 knockdown inhibits PDAC cell proliferation, tumor growth, and metastasis.
- PRSS23 regulates the Hippo signaling pathway by modulating the PP2A-MST1 interaction, affecting YAP activity.
Conclusions:
- PRSS23 is a critical oncogene and a potential prognostic biomarker for PDAC.
- PRSS23 promotes PDAC tumorigenesis and metastasis via the PP2A-MST1-YAP axis.
- Targeting the PRSS23/PP2A/MST1 pathway presents a promising therapeutic avenue for PDAC.
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