Yang TF, Li XR, Kong MW. Molecular mechanisms underlying roles of long non-coding RNA small nucleolar RNA host gene 16 in digestive system cancers. World J Gastrointest Oncol 2024; 16(11): 4300-4308 [PMID: 39554746 DOI: 10.4251/wjgo.v16.i11.4300]
Corresponding Author of This Article
Mo-Wei Kong, MD, Doctor, Department of Cardiology, Guiqian International General Hospital, No. 1 Dongfeng Avenue, Wudang District, Guiyang 550018, Guizhou Province, China. 1600181272@qq.com
Research Domain of This Article
Oncology
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 Gastrointest Oncol. Nov 15, 2024; 16(11): 4300-4308 Published online Nov 15, 2024. doi: 10.4251/wjgo.v16.i11.4300
Molecular mechanisms underlying roles of long non-coding RNA small nucleolar RNA host gene 16 in digestive system cancers
Ting-Fang Yang, Xin-Rui Li, Mo-Wei Kong
Ting-Fang Yang, Department of Oncology, Guiqian International General Hospital, Guiyang 550018, Guizhou Province, China
Xin-Rui Li, Mo-Wei Kong, Department of Cardiology, Guiqian International General Hospital, Guiyang 550018, Guizhou Province, China
Co-first authors: Ting-Fang Yang and Xin-Rui Li.
Author contributions: Yang TF and Li XR contributed equally to this work as co-first authors; Kong MW provided crucial suggestions and guidance for manuscript writing; Yang TF wrote the manuscript; Li XR reviewed and revised the manuscript; and all authors read and approved the final manuscript.
Conflict-of-interest statement: The authors have no conflicts of interest to declare that are relevant to the content of this article.
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: Mo-Wei Kong, MD, Doctor, Department of Cardiology, Guiqian International General Hospital, No. 1 Dongfeng Avenue, Wudang District, Guiyang 550018, Guizhou Province, China. 1600181272@qq.com
Received: February 25, 2024 Revised: June 13, 2024 Accepted: July 2, 2024 Published online: November 15, 2024 Processing time: 242 Days and 21.5 Hours
Abstract
This editorial reviews the molecular mechanisms underlying the roles of the long non-coding RNA (lncRNA) small nucleolar RNA host gene 16 (SNHG16) in digestive system cancers based on two recent studies on lncRNAs in digestive system tumors. The first study, by Zhao et al, explored how hBD-1 affects colon cancer, via the lncRNA TCONS_00014506, by inhibiting mTOR and promoting autophagy. The second one, by Li et al, identified the lncRNA prion protein testis specific (PRNT) as a factor in oxaliplatin resistance by sponging ZNF184 to regulate HIPK2 and influence colorectal cancer progression and chemoresistance, suggesting PRNT as a potential therapeutic target for colorectal cancer. Both of these two articles discuss the mechanisms by which lncRNAs contribute to the development and progression of digestive system cancers. As a recent research hotspot, SNHG16 is a typical lncRNA that has been extensively studied for its association with digestive system cancers. The prevailing hypothesis is that SNHG16 participates in the development and progression of digestive system tumors by acting as a competing endogenous RNA, interacting with other proteins, regulating various genes, and affecting downstream target molecules. This review systematically examines the recently reported biological functions, related molecular mechanisms, and potential clinical significance of SNHG16 in various digestive system cancers, and explores the relationship between SNHG16 and digestive system cancers. The findings suggest that SNHG16 may serve as a potential biomarker and therapeutic target for human digestive system cancers.
Core Tip: The long non-coding RNA (lncRNA) small nucleolar RNA host gene 16 (SNHG16) plays a significant role in the development and progression of various digestive system cancers, including esophageal, liver, pancreatic, gastric, and colorectal cancers. It is involved in processes such as cell proliferation, migration, invasion, apoptosis, and chemoresistance. SNHG16 acts as a competing endogenous RNA, interacting with microRNAs and regulating target genes, and is associated with a poor prognosis in digestive system cancers. Its expression is influenced by transcription factors and its polymorphisms are linked to cancer susceptibility. SNHG16 has potential as a biomarker and therapeutic target for digestive system cancers.
