Jin XS, Chen LX, Ji TT, Li RZ. SERPINH1 promoted the proliferation and metastasis of colorectal cancer by activating PI3K/Akt/mTOR signaling pathway. World J Gastrointest Oncol 2024; 16(5): 1890-1907 [PMID: 38764814 DOI: 10.4251/wjgo.v16.i5.1890]
Corresponding Author of This Article
Rong-Zhou Li, MD, Professor, Department of Gastroenterology, The Third Affiliated Hospital of Wenzhou Medical University, No. 108 Wansong Road, Ruian 325000, Zhejiang Province, China. lrz23228@163.com
Research Domain of This Article
Oncology
Article-Type of This Article
Clinical and Translational Research
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (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: http://creativecommons.org/licenses/by-nc/4.0/
World J Gastrointest Oncol. May 15, 2024; 16(5): 1890-1907 Published online May 15, 2024. doi: 10.4251/wjgo.v16.i5.1890
SERPINH1 promoted the proliferation and metastasis of colorectal cancer by activating PI3K/Akt/mTOR signaling pathway
Xiao-Sheng Jin, Lu-Xi Chen, Ting-Ting Ji, Rong-Zhou Li
Xiao-Sheng Jin, Lu-Xi Chen, Ting-Ting Ji, Rong-Zhou Li, Department of Gastroenterology, The Third Affiliated Hospital of Wenzhou Medical University, Ruian 325000, Zhejiang Province, China
Author contributions: Jin XS, Chen LX, Ji TT, and Li RZ designed the research; Jin XS performed the research and wrote the paper; Li RZ supervised the report; Chen LX contributed to the analysis; Ji TT provided constructive advice; and all the authors read and approved the final manuscript.
Institutional review board statement: This study was approved by the Ethics Committee of the Third Affiliated Hospital of Wenzhou Medical University, No. YJ2022043.
Clinical trial registration statement: This study did not involve any clinical trials.
Informed consent statement: The specimens involved in this study have been obtained with signed informed consent from the patients.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Data sharing statement: The original contributions presented in the study are included in the article materials. Further inquiries can be directed to the corresponding authors.
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: Rong-Zhou Li, MD, Professor, Department of Gastroenterology, The Third Affiliated Hospital of Wenzhou Medical University, No. 108 Wansong Road, Ruian 325000, Zhejiang Province, China. lrz23228@163.com
Received: October 19, 2023 Peer-review started: October 19, 2023 First decision: December 29, 2023 Revised: January 10, 2024 Accepted: March 14, 2024 Article in press: March 14, 2024 Published online: May 15, 2024 Processing time: 202 Days and 21.5 Hours
ARTICLE HIGHLIGHTS
Research background
The clinical significance and biological role of serpin peptidase inhibitor clade H member 1 (SERPINH1) in colorectal cancer (CRC) remains poorly understood.
Research motivation
To investigate the effect of SERPINH1 on CRC cells and its specific mechanism.
Research objectives
To further study the specific role and mechanism of SERPINH1 in CRC and provide theoretical basis for further using SERPINH1 to improve the survival rate of CRC patients.
Research methods
SERPINH1 expression in CRC cell lines and tissues was evaluated using quantitative real-time polymerase chain reaction, western blotting analysis, data mining from The Cancer Genome Atlas, and immunohistochemistry. A battery of in vitro experiments was conducted to elucidate the role of SERPINH1 and its potential mechanisms in CRC.
Research results
Our study reveals the potential for SERPINH1 to be negatively correlated with fatty acid metabolism and promote CRC progression by activating the phosphatidylinositol 3-kinase (PI3K)/AKT/mechanistic target of rapamycin (mTOR) and PI3K/AKT/FOXO1 pathways. Considering that FOXO1 and glycogen synthase kinase (GSK)-3β phosphorylation can inhibit fatty acid metabolism, which is partly mediated by CD36, this may be our next research direction.
Research conclusions
Our study uncovered the significance of SERPINH1 in promoting CRC proliferation and metastasis by activating the PI3K/Akt/mTOR pathway. This work contributes to our understanding of the molecular mechanisms underlying CRC progression and offers a potential avenue for the development of targeted therapies.
Research perspectives
Our study revealed the potential for SERPINH1 to be negatively correlated with fatty acid metabolism and promoted CRC progression by activating the PI3K/AKT/mTOR and PI3K/AKT/FOXO1 pathways. Considering that FOXO1 and GSK-3β phosphorylation could inhibit fatty acid metabolism, which is partly mediated by CD36, this may be our next research direction.
