Kong MW, Li XR, Gao Y, Yang TF. Tumor-related factor complement Clq/TNF-related protein 6 affects the development of digestive system tumors through the phosphatidylinositol 3-kinase pathway. World J Gastroenterol 2024; 30(26): 3206-3209 [PMID: 39086639 DOI: 10.3748/wjg.v30.i26.3206]
Corresponding Author of This Article
Ting-Fang Yang, MA, Doctor, Department of Oncology, Guiqian International General Hospital, No. 1 Dongfeng Avenue, Wudang District, Guiyang 550018, Guizhou Province, China. 672539517@qq.com
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
Editorial
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 Gastroenterol. Jul 14, 2024; 30(26): 3206-3209 Published online Jul 14, 2024. doi: 10.3748/wjg.v30.i26.3206
Tumor-related factor complement Clq/TNF-related protein 6 affects the development of digestive system tumors through the phosphatidylinositol 3-kinase pathway
Mo-Wei Kong, Xin-Rui Li, Yu Gao, Ting-Fang Yang
Mo-Wei Kong, Xin-Rui Li, Department of Cardiology, Guiqian International General Hospital, Guiyang 550018, Guizhou Province, China
Yu Gao, Department of Endocrinology, The Affiliated Hospital of Chengde Medical College, Chengde 067000, Hebei Province, China
Ting-Fang Yang, Department of Oncology, Guiqian International General Hospital, Guiyang 550018, Guizhou Province, China
Co-first authors: Mo-Wei Kong and Xin-Rui Li.
Author contributions: Li XR and Kong MW contributed equally; Li XR and Gao Y provided crucial suggestions and guidance for the writing; Kong MW wrote the manuscript; Yang TF reviewed and revised the manuscript; All authors read and approved the final manuscript.
Conflict-of-interest statement: The authors declare that they have no competing interests.
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: Ting-Fang Yang, MA, Doctor, Department of Oncology, Guiqian International General Hospital, No. 1 Dongfeng Avenue, Wudang District, Guiyang 550018, Guizhou Province, China. 672539517@qq.com
Received: May 6, 2024 Revised: June 3, 2024 Accepted: June 19, 2024 Published online: July 14, 2024 Processing time: 64 Days and 5.2 Hours
Abstract
In this editorial, we review the work of Razali et al published in World J Gastroenterology, with a particular focus on the effect of rs10889677 variation in the phosphatidylinositol 3-kinase (PI3K) pathway and buparlisib on colitis-associated cancer. The role of PI3K in promoting cancer progression has been widely recognized, as it is involved in regulating the survival, differentiation, and proliferation of cancer cells. The complement Clq/TNF-related protein 6 (CTRP6) is a newer tumor-associated factor. Recent studies have revealed the pro-tumor effect of CTRP6 in gastric cancer, hepatocellular carcinoma, colorectal cancer, and other gastrointestinal tumors through the PI3K pathway. This article attempts to reveal the mechanism through which the CTRP6 affects the development of digestive system tumors through the PI3K pathway by summarizing recent research.
Core Tip: The complement Clq/TNF-related protein 6 (CTRP6), a member of the CTRP family, is increasingly recognized for its role in the development of digestive system tumors, particularly through its interaction with the phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway. This pathway is a key regulator of cell growth, survival, and metabolism, and its dysregulation is a common feature in various cancers. In gastric, colorectal, and liver cancers, CTRP6 has been shown to promote tumor progression by activating the PI3K/Akt pathway, leading to increased cell proliferation, migration, and angiogenesis. Targeting CTRP6 or its downstream signaling components could offer a novel therapeutic strategy for these malignancies. Further research is essential to fully understand the role of CTRP6 in tumorigenesis and to develop targeted therapies that exploit its influence on the PI3K/Akt pathway.
