ArticleJournal of advanced research2025
Enhanced LRP8 expression induced by Helicobacter pylori drives gastric cancer progression by facilitating β-Catenin nuclear translocation.
Article in Journal of advanced research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 16 citations in OpenAlex.
- Gastrointestinal Microbiome Dysbiosis in Cancer Development: Mechanisms and Biomarker Potential.MicrobiologyOpen · 2026Review
- Advances inOncology letters · 2026Review
- LRP8 Promotes colorectal cancer progression by suppressing ferroptosis through the SLC3A2/GPX4 signalling axis.European journal of medical research · 2026Article
- Patient-derived organoids in gastric cancer: bridging the tumor microenvironment to functional precision oncology.Frontiers in bioengineering and biotechnology · 2026Review
- Integrated transcriptomics and molecular docking identify hub genes and statin regulators inFrontiers in cellular and infection microbiology · 2026Article
- Nuclear β-catenin: molecular regulation, challenges and therapeutic opportunities.Cell communication and signaling : CCS · 2025Review
- Article
- KRT23 promotes proliferation invasion and metastasis of gastric cancer through epithelial-mesenchymal transition mediated by the PI3K/AKT/mTOR signaling pathway.Translational cancer research · 2025Article
- LRP8 Regulates Lipid Metabolism to Stimulate Malignant Progression and Cisplatin Resistance in Bladder Cancer.The Kaohsiung journal of medical sciences · 2025Article
- The application of organoids in treatment decision-making for digestive system cancers: progress and challenges.Molecular cancer · 2025Review
- The regulation of LRPs by miRNAs in cancer: influencing cancer characteristics and responses to treatment.Cancer cell international · 2025Review
- LRP11 facilitates lipid metabolism and malignancy in hepatocellular carcinoma by stabilizing RACK1 through USP5 regulation.Molecular medicine (Cambridge, Mass.) · 2025Article
- Helicobacter pylori and gastric cancer: mechanisms and new perspectives.Journal of hematology & oncology · 2025Review
- The intersection ofFrontiers in cellular and infection microbiology · 2025Review
- Organoids: development and applications in disease models, drug discovery, precision medicine, and regenerative medicine.MedComm · 2024Review
Corrections and comments
- Erratum issued
Authors and funding
15 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionHelicobacter pylori (H. pylori) infection has been associated with gastric carcinogenesis. However, the precise involvement of LRP8, the low-density lipoprotein receptor-related protein 8, in H. pylori pathogenesis and gastric cancer (GC) remains poorly understood.
objectivesTo investigate the potential role of LRP8 in H. pylori infection and gastric carcinogenesis.
methodsThree-dimensional human-derived gastric organoids (hGO) and gastric cancer organoids (hGCO) were synthesized from the tissues obtained from human donors. In this work, multi-omics combined with in vivo and in vitro studies were conducted to investigate the potential involvement of LRP8 in H. pylori-induced GC.
resultsWe found that H. pylori infection significantly upregulated the expression of LRP8 in human GC tissues, cells, organoids, and mouse gastric mucous. In particular, LRP8 exhibited a distinct enrichment in cancer stem cells (CSC). Functionally, silencing of LRP8 affected the formation and proliferation of tumor spheroids, while increased expression of LRP8 was associated with increased proliferation and stemness of GC cells and organoids. Mechanistically, LRP8 promotes the binding of E-cadherin to β-catenin, thereby promoting nuclear translocation and transcriptional activity of β-catenin. Furthermore, LRP8 interacts with the cytotoxin-associated gene A (CagA) to form the CagA/LRP8/β-catenin complex. This complex further amplifies H. pylori-induced β-catenin nuclear translocation, leading to increased transcription of inflammatory factors and CSC markers. Clinical analysis demonstrated that abnormal overexpression of LRP8 is correlated with a poor prognosis and resistance to 5-Fluorouracil in patients with GC.
conclusionOur findings provide valuable information on the molecular intricacies of H. pylori-induced gastric carcinogenesis, offering potential therapeutic targets and prognostic markers for GC.
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