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©The Author(s) 2025. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Diabetes. Jun 15, 2025; 16(6): 102727
Published online Jun 15, 2025. doi: 10.4239/wjd.v16.i6.102727
Published online Jun 15, 2025. doi: 10.4239/wjd.v16.i6.102727
Mechanism of trypsin-mediated differentiation of pancreatic progenitor cells into functional islet-like clusters
Ling Gao, Jia-Shuang Lai, Li-Xia Qian, Wan-Jin Hong, Liang-Cheng Li, Fujian Provincial Key Laboratory of Innovative Drug Target Research, School of Pharmaceutical Sciences, Xiamen University, Xiamen 361102, Fujian Province, China
Han Chen, Department of Pharmacology, Division of Biosciences, University College London, London WC1E 6BT, United Kingdom
Co-corresponding authors: Wan-Jin Hong and Liang-Cheng Li.
Author contributions: Gao L and Lai JS designed the study, conducted the experiments, and drafted the manuscript; Chen H reviewed the manuscript; Qian LX researched the data; Hong WJ and Li LC conceived the project, designed the experiments, reviewed the results, and wrote the manuscript.
Supported by the National Natural Science Foundation of China, No. 82073908.
Institutional review board statement: This study does not involve any human experiments, as is based on previous experiments, we conducted mechanistic studies using pancreatic cancer cell lines with pancreatic progenitor/progenitor cell properties.
Institutional animal care and use committee statement: This manuscript does not involve animal experiments.
Conflict-of-interest statement: The authors have no conflicts of interest to declare.
Data sharing statement: The datasets generated from the current study are available from the corresponding author upon reasonable request.
Open Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Liang-Cheng Li, PhD, Professor, Fujian Provincial Key Laboratory of Innovative Drug Target Research, School of Pharmaceutical Sciences, Xiamen University, No. 4221-115 Xiangan South Road, Xiangan District, Xiamen 361102, Fujian Province, China. lchli2013@xmu.edu.cn
Received: October 28, 2024
Revised: January 20, 2025
Accepted: March 28, 2025
Published online: June 15, 2025
Processing time: 229 Days and 11.2 Hours
Revised: January 20, 2025
Accepted: March 28, 2025
Published online: June 15, 2025
Processing time: 229 Days and 11.2 Hours
Core Tip
Core Tip: Trypsin induced pancreatic cancer cell line-1 cell differentiation into insulin-producing cells. Loss of E-cadherin, αE-catenin, and casein kinase-1γ3 (CK1γ3) blocked trypsin-induced differentiation. Hydrolysis of E-cadherin by trypsin recruited CK1γ3. CK1γ3 phosphorylated αE-catenin at Ser655/Thr658.