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©The Author(s) 2024. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastrointest Oncol. Mar 15, 2024; 16(3): 1029-1045
Published online Mar 15, 2024. doi: 10.4251/wjgo.v16.i3.1029
Published online Mar 15, 2024. doi: 10.4251/wjgo.v16.i3.1029
CALD1 facilitates epithelial-mesenchymal transition progression in gastric cancer cells by modulating the PI3K-Akt pathway
Wen-Qian Ma, Shuo Guo, Li-Mian Er, Department of Endoscopy, The Fourth Hospital of Hebei Medical University, Shijiazhuang 050011, Hebei Province, China
Wen-Qian Ma, Ping-An Ding, Bi-Bo Tan, Wen-Bo Liu, Shuo Guo, Li-Mian Er, Zhi-Dong Zhang, Qun Zhao, Hebei Key Laboratory of Precision Diagnosis and Comprehensive Treatment of Gastric Cancer, Shijiazhuang 050011, Hebei Province, China
Ming-Chang Miao, Department of Radiotherapy, The Fourth Hospital of Hebei Medical University, Shijiazhuang 050011, Hebei Province, China
Ping-An Ding, Bi-Bo Tan, Wen-Bo Liu, Zhi-Dong Zhang, Qun Zhao, The Third Department of Surgery, The Fourth Hospital of Hebei Medical University, Shijiazhuang 050011, Hebei Province, China
Author contributions: Ma WQ, Tan BB, and Liu WB designed the study; Ma WQ and Liu WB wrote the manuscript; Ma WQ, Ding PA, Liu WB, and Guo S performed the experiments; Ma WQ, Miao MC, and Er LM analyzed the data; Zhang ZD and Zhao Q reviewed and edited the manuscript; all authors have read and approved the final manuscript.
Supported by The Hebei Provincial Major Science and Technology Special Project , No. 23297701Z ; Beijing-Tianjin-Hebei Basic Research Cooperation Special Project , No. 22JCZXJC00140 ; Hebei Provincial Government-Funded Clinical Talent Project , No. ZF2023047 .
Institutional review board statement: The study was approved by the Ethics Committee of the Fourth Hospital of Hebei Medical University.
Conflict-of-interest statement: The authors declare that they have no competing interests to disclose.
Data sharing statement: The datasets used and analyzed during the current study are available from the corresponding author on 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: Qun Zhao, MD, PhD, Chief Doctor, Professor, The Third Department of Surgery, The Fourth Hospital of Hebei Medical University, No. 12 Jiankang Road, Changan District, Shijiazhuang 050011, Hebei Province, China. zhaoqun@hebmu.edu.cn
Received: November 22, 2023
Peer-review started: November 22, 2023
First decision: December 8, 2023
Revised: December 21, 2023
Accepted: January 4, 2024
Article in press: January 4, 2024
Published online: March 15, 2024
Processing time: 111 Days and 1.2 Hours
Peer-review started: November 22, 2023
First decision: December 8, 2023
Revised: December 21, 2023
Accepted: January 4, 2024
Article in press: January 4, 2024
Published online: March 15, 2024
Processing time: 111 Days and 1.2 Hours
Core Tip
Core Tip: In this study, the relationship between CALD1 and gastric cancer (GC) and the possible network regulatory mechanisms of CALD1 were explored by bioinformatics methods and validated by experiments. We conducted functional analysis and verification through tissue and cell experiments, delving into possible pathways and mechanisms involved. It was showed that CALD1 may participate in the proliferation, invasion, and migration, and epithelial-mesenchymal transition (EMT)-related gene and protein expression in GC cells. Our study suggested that CALD1, through PI3K-Akt signaling pathway activation, may regulate EMT in GC cells, representing a potentially novel target for GC treatment.