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
Core Tip
Core Tip: The expression of serpin peptidase inhibitor clade H member 1 (SERPINH1) was observed to be elevated in both colorectal cancer (CRC) cells and tissues at mRNA and protein levels. Increased SERPINH1 expression demonstrated a close association with the T stage, lymph node status, and distant metastasis in CRC patients, displaying a significant correlation with poor overall survival. Subsequent investigations revealed that the overexpression of SERPINH1 markedly enhanced the in vitro proliferation, invasion, and migration capabilities of CRC cells. Conversely, the knockdown of SERPINH1 resulted in the opposite effects. In addition, our study validated that the overexpression of SERPINH1 could stimulate the G1/S phase cell cycle transition through the activation of the phosphatidylinositol 3-kinase (PI3K)/AKT/mechanistic target of rapamycin (mTOR) pathways. Additionally, it was observed that the overexpression of SERPINH1 facilitated cell invasion and migration by modulating the PI3K/AKT/mTOR pathway. These findings emphasize the pivotal role of SERPINH1 in promoting CRC progression, providing insights into its potential as a therapeutic target for CRC treatment.
