Molecular mechanisms underlying roles of long non-coding RNA small nucleolar RNA host gene 16 in digestive system cancers

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.

Keywords: Digestive system cancers; Long non-coding RNAs; Small nucleolar RNA host gene 16; Colon cancer

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.