Role of long non-coding RNAs in the pathogenesis of gastric cancer-induced by Helicobacter pylori.

Abstract

Gastric cancer (GC) remains a significant global health burden with Helicobacter pylori (H. pylori) infection considered a primary risk factor. However, the precise molecular mechanisms of this relationship are still being elucidated. Recent studies have revealed that long non-coding RNAs (lncRNAs) play a crucial role in regulating gene expression, significantly impacting various biological processes, including carcinogenesis. LncRNAs are non-protein-coding transcripts that are over 200 nucleotides long. It has been reported that lncRNAs play a dual role, in promoting or inhibiting cancer progression through intricate molecular pathways in H. pylori-associated GC. The aim of this study was to provide an overview of the role of lncRNAs in the pathogenesis of GC induced by H. pylori. Upregulated lncRNAs such as H19, GClnc1, LINC00152, and PVT1 in H. pylori-infected patients contribute to tumorigenesis by enhancing cell proliferation, migration, invasion, and inflammation. This is often achieved through interactions with oncogenic pathways, stabilization of pro-tumor proteins, or acting as sponges for tumor-suppressive microRNAs. The mechanisms of lncRNA action are diverse, encompassing epigenetic, transcriptional, and post-transcriptional regulation, as well as influencing protein interactions and key signaling pathways, such as Wnt/β-catenin, PI3K/AKT, and NF-κB. Furthermore, lncRNAs are implicated in DNA damage and genomic instability induced by H. pylori, as well as in creating the tumor microenvironment by regulating angiogenesis and immune evasion. This multifaceted involvement positions lncRNAs as promising diagnostic, prognostic, and therapeutic markers for H. pylori-associated GC, warranting further investigation for novel clinical interventions.