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Updated: Jun 5, 2026

Oncogene Expression Analysis with Alterations in pH in a Pancreatic Ductal Cell Line
Published on: April 11, 2025
The OAS1-FASN axis promotes pancreatic cancer by coordinating lipogenic stress and the unfolded protein response
Yuheng Zhu1, Hongfei Yao1, Chunjing Li1
1Department of Hepato‑Biliary‑Pancreatic Surgery, General Surgery, Huadong Hospital, Fudan University, Shanghai, PR China.
Abstract:
Metabolic reprogramming, characterized by dysregulated lipid metabolism and consequent endoplasmic reticulum (ER) stress, constitutes a hallmark of pancreatic ductal adenocarcinoma (PDAC). Within this metabolic landscape, the 2'-5'-Oligoadenylate Synthetase (OAS) family member OAS1 is identified as a critical driver of malignancy, exhibiting specific upregulation in PDAC tissues that correlates with poor patient prognosis. Functionally, OAS1 drives tumor progression, including cell proliferation and metastasis, by operating as a non-canonical metabolic regulator. Mechanistically, OAS1 binds to fatty acid synthase (FASN), maintaining its functional protein levels and thereby promoting FASN-dependent lipid synthesis. The resulting surge in de novo lipid synthesis and lipid droplet accumulation precipitates an adaptive ER stress response via the PERK-ATF4 signaling axis. Consequently, a functional OAS1-FASN axis operates to coordinate lipid overload with pro-survival ER stress signaling, establishing OAS1 as a pivotal metabolic regulator and a viable biomarker in PDAC.
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