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©The Author(s) 2023. Published by Baishideng Publishing Group Inc. All rights reserved.
LINC01268 promotes epithelial-mesenchymal transition, invasion and metastasis of gastric cancer via the PI3K/Akt signaling pathway and targeting MARCKS
Ling-Han Tang, Peng-Cheng Ye, Lin Yao, Ya-Jun Luo, Wang Tan, Wan-Ping Xiang, Zi-Lin Liu, Ling Tan, Jiang-Wei Xiao
Ling-Han Tang, Zi-Lin Liu, Jiang-Wei Xiao, Department of Gastrointestinal Surgery, Clinical Medical College and the First Affiliated Hospital of Chengdu Medical College, Chengdu 610000, Sichuan Province, China
Peng-Cheng Ye, Lin Yao, Department of Gastrointestinal Surgery, The Affiliated Hospital of North Sichuan Medical College, Nanchong 637000, Sichuan Province, China
Ya-Jun Luo, Department of Gastrointestinal Surgery, Sichuan Cancer Hospital, Chengdu 610000, Sichuan Province, China
Wang Tan, Department of Gastrointestinal Surgery, Yaan People’s Hospital, Yaan 625000, Sichuan Province, China
Wan-Ping Xiang, Department of Thoracic Surgery, The Affiliated Hospital of North Sichuan Medical College, Nanchong 637000, Sichuan Province, China
Ling Tan, Department of Surgery, People’s Hospital Affiliated to Chongqing Three Gorges Medical College, Chongqing 404041, China
Author contributions: Tang LH and Xiao JW conceived and designed the experiments; Tang LH and Ye PC did most of the experiments and data analysis; Tang LH wrote the manuscript; Ye PC, Luo YJ, Yao L and Liu ZL collected the clinical data; Tan W, Xiang WP and Tan L performed data analysis; Xiao JW revised the manuscript; and all authors have read and approved the final manuscript.
Supported by the National Natural Science Foundation of China, No. 81070378 and 81270561; and Natural Science Foundation of Sichuan Province, China, No. 2022NSFSC0050 and 2023NSFSC1896.
Institutional review board statement: The study was reviewed and approved by the Ethics Committee of the Affiliated Hospital of North Sichuan Medical College.
Informed consent statement: All gastric cancer patients and healthy volunteers provided written informed consent.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Data sharing statement: No additional data are available.
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: Jiang-Wei Xiao, MD, PhD, Doctor, Professor, Surgeon, Department of Gastrointestinal Surgery, Clinical Medical College and the First Affiliated Hospital of Chengdu Medical College, No. 278 Baoguang Road, Xindu District, Chengdu 610000, Sichuan Province, China.
xiaojiangwei2018@163.com
Received: February 12, 2023
Peer-review started: February 12, 2023
First decision: March 28, 2023
Revised: April 11, 2023
Accepted: June 19, 2023
Article in press: June 19, 2023
Published online: August 15, 2023
Processing time: 178 Days and 23.8 Hours
BACKGROUND
Long non-coding RNAs (lncRNAs) with differential expression characteristics have been found to be closely related to the tumorigenesis and development of gastric cancer (GC), but their specific mechanisms and roles still need to be further elucidated.
AIM
To investigate the expression of LINC01268 in GC and its mechanism of affecting GC progression.
METHODS
Real-time quantitative polymerase chain reaction was used to detect the expression of LINC01268 in GC tissues, cell lines and plasma. The Kaplan-Meier method was used to evaluate the value of LINC01268 in the prognostication of GC patients. An receiver operating characteristic curve was constructed to evaluate the value of LINC01268 in the diagnosis of GC. Transwell migration and invasion assays and wound healing assays were used to confirm the effect of LINC01268 on the invasion and migration of GC cells. The regulatory relationship between LINC01268 and myristoylated alanine rich protein kinase C substrate (MARCKS), the PI3K/Akt signaling pathway, and the epithelial-mesenchymal transition (EMT) process in GC was demonstrated by western blot analysis.
RESULTS
The expression of LINC01268 was increased in GC tissues and cell lines. The expression level of LINC01268 was significantly correlated with lymph node metastasis, TNM stage, and tumor differentiation in patients with GC. Over-expression of LINC01268 indicated a poor prognosis for patients with GC, and it had a certain auxiliary diagnostic value for GC. In vitro functional experiments proved that the abnormal expression of LINC01268 further activated the PI3K/Akt signaling pathway and promoted EMT by targeting and regulating MARCKS and ultimately promoted the invasion and metastasis of GC.
CONCLUSION
This study elucidates that LINC01268 in GC may be an oncogene that further activates the PI3K/Akt signaling pathway and EMT by targeting and regulating MARCKS, and ultimately promotes the invasion and metastasis of GC. LINC01268 may be a potential effective target for the treatment of GC.
Core Tip: Overexpression of LINC01268 was related to the prognosis of patients with gastric cancer (GC) and showed the value of auxiliary diagnosis. Overexpression of LINC01268 promoted the invasion and metastasis of GC cells. LINC01268 activated the PI3K/Akt signaling pathway and promoted epithelial-mesenchymal transition by targeting myristoylated alanine rich protein kinase C substrate and ultimately promoted the invasion and metastasis of GC.
