ReviewInflammopharmacology2025
Role of long non-coding RNAs in the pathogenesis of gastric cancer-induced by Helicobacter pylori.
Review in Inflammopharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Advances inOncology letters · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.