RACK1 attenuates pancreatic tumorigenesis by suppressing acinar-to-ductal metaplasia through inflammatory signaling modulation
RACK1 serves as a gatekeeper restraining inflammation-driven ADM transformation, with its downregulation constituting an early molecular event in PDA pathogenesis. The RACK1-MAP2K3 axis orchestrates malignant transition through simultaneous NF-κB activation (inflammatory priming) and MAPK hyperactivation (proliferative drive). Our findings nominate RACK1 as both a stratification biomarker for high-risk pancreatic lesions and a druggable node for intercepting preneoplastic progression.
Authors
- Keping Xie (ORCID: https://orcid.org/0000-0001-7887-9586)
- Huiqing Zhang (ORCID: https://orcid.org/0009-0002-3732-6832)
- Wei Fang (ORCID: https://orcid.org/0000-0002-2889-9463)
- Wei Zhang (ORCID: https://orcid.org/0000-0002-2358-0779)
- Tingting Jiang (ORCID: https://orcid.org/0000-0002-5372-0656)
- Xiaojia Li
Institutions
- Jiangxi Provincial Cancer Hospital (CN)
- South China University of Technology (CN)
Publication Details
- Journal
- Cellular Oncology
- Published
- 2025-09-01
- DOI
- https://doi.org/10.1007/s13402-025-01084-3
- Citations
- 1
- Primary Topic
- Pancreatic and Hepatic Oncology Research
- Type
- article
- Field-Weighted Citation Impact
- 1.05
Funders
- National Natural Science Foundation of China
- Natural Science Foundation of Guangdong Province
- South China University of Technology