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©The Author(s) 2024. Published by Baishideng Publishing Group Inc. All rights reserved.
CALD1 facilitates epithelial-mesenchymal transition progression in gastric cancer cells by modulating the PI3K-Akt pathway
Wen-Qian Ma, Ming-Chang Miao, Ping-An Ding, Bi-Bo Tan, Wen-Bo Liu, Shuo Guo, Li-Mian Er, Zhi-Dong Zhang, Qun Zhao
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
ARTICLE HIGHLIGHTS
Research background
CALD1 is known for its abnormal expression in various malignant tumors, and this expression is linked to tumor growth and immune system infiltration. However, the specific functions and underlying mechanisms of CALD1 in the epithelial-mesenchymal transition (EMT) process in gastric cancer (GC) remain unclear.
Research motivation
The motivation behind this research is to explore and better comprehend how CALD1 functions in the context of GC.
Research objectives
This study aimed to investigate the role and mechanism of CALD1 in GC progression, invasion, and migration.
Research methods
In this study, the relationship between CALD1 and GC, as well as the possible network regulatory mechanisms of CALD1, was investigated by bioinformatics and validated by experiments. CALD1-siRNA was synthesized and used to transfect GC cells. Cell activity was measured using the CCK-8 method, cell migration and invasive ability were measured using wound healing assay and Transwell assay, and the expression levels of relevant genes and proteins in each group of cells were measured using qRT-PCR and Western blot. A GC cell xenograft model was established to verify the results of in vitro experiments.
Research results
The bioinformatics analysis revealed that CALD1 expression was significantly elevated in GC tissues, particularly in the EMT type. Additionally, the CALD1 gene was found to be associated with the PI3K-Akt signaling pathway and other EMT components. Compared to gastric epithelial cell lines, GC cell lines showed higher levels of CALD1 expression. Suppressing CALD1 and the PI3K-Akt pathway resulted in reduced viability, invasion, and migration of GC cells. These experimental findings elucidate the role of CALD1 and the PI3K-Akt pathway in GC, laying a foundation for further molecular mechanism studies of this disease.
Research conclusions
By influencing the PI3K-Akt pathway, CALD1 plays a pivotal role in advancing the EMT in GC.
Research perspectives
This study, through bioinformatics analysis, as well as in vivo and in vitro experiments, has confirmed that CALD1 promotes the EMT in GC by affecting the PI3K-Akt signaling pathways. These findings underscore its significance in tumor progression and potential as a target for future therapeutic approaches. However, the investigation into the regulatory function of these pathways in this research was not comprehensive, leaving the full mechanism of action somewhat unclear. To validate the study's conclusions more robustly, further research involving a larger patient cohort is necessary.
