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Copyright: ©Author(s) 2026. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution-NonCommercial (CC BY-NC 4.0) license. No commercial re-use. See permissions. Published by Baishideng Publishing Group Inc.
World J Gastroenterol. Nov 21, 2026; 32(43): 119315
Published online Nov 21, 2026. doi: 10.3748/wjg.v32.i43.119315
RHEB-CSF1R signaling, autophagy, and metastatic plasticity in pancreatic cancer: Current advances, controversies, and translational opportunities
Jun-Xia Hu, Ye Zhang, Yue-Mei Chen, Lei Cao
Jun-Xia Hu, Ye Zhang, Yue-Mei Chen, Lei Cao, Department of Oncology, Jiangsu Province (Suqian) Hospital, Suqian 223800, Jiangsu Province, China
Lei Cao, Department of Oncology, Suqian Clinical Medical College of Jiangsu University, Suqian 223800, Jiangsu Province, China
Author contributions: Hu JX, Zhang Y, and Chen YM contributed to language editing, formatting, and reference checking, and provided topic-focused input (phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin and autophagy) to refine the discussion; Cao L wrote the manuscript and is responsible for the overall content; and all authors reviewed and approved the final manuscript.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Corresponding author: Lei Cao, PhD, Chief Physician, Professor, Department of Oncology, Jiangsu Province (Suqian) Hospital, No. 120 Suzhi Road, Sucheng District, Suqian 223800, Jiangsu Province, China. brawnym80@163.com
Received: January 26, 2026
Revised: March 9, 2026
Accepted: May 6, 2026
Published online: November 21, 2026
Processing time: 244 Days and 3.5 Hours
Core Tip

Core Tip: A recent study comprehensively summarized that a tumor-cell ras homolog enriched in brain-colony stimulating factor 1 receptor complex promotes pancreatic cancer metastasis by increasing phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin phosphorylation, suppressing autophagy, and inducing epithelial-mesenchymal transition. Building on this work, the present article discusses how ras homolog enriched in brain-centered signaling may connect tumor-cell metabolic adaptation, macrophage-associated biology, autophagy regulation, and metastatic plasticity in pancreatic ductal adenocarcinoma. We emphasize current advances, major controversies, and translational opportunities, with particular focus on tumor-cell colony stimulating factor 1 receptor, autophagic flux, and biomarker-guided therapeutic development.

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