ArticleBiomolecules2022
Alteration of Cellular Energy Metabolism through LPAR2-Axin2 Axis in Gastric Cancer.
Article in Biomolecules, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 7 citations in OpenAlex.
- Review
- miR-3614-5p prevents endothelial differentiation and angiogenesis in human exfoliated deciduous teeth by targeting lysophosphatidic acid receptor 2.In vitro cellular & developmental biology. Animal · 2026Article
- Identification of a lactylation-related gene signature in microsatellite stable gastric cancer based on bulk and single-cell RNA-seq.Frontiers in immunology · 2026Article
- Integrated analysis of cell-in-cell related genes and immune microenvironment in heart failure.Frontiers in cell and developmental biology · 2026Article
- Decoding lysophosphatidic acid signaling in physiology and disease: mapping the multimodal and multinodal signaling networks.Signal transduction and targeted therapy · 2025Review
- CYMP-AS1 Promotes Ovarian Cancer Progression by Enhancing the Intracellular Translocation of hnRNPM and Reducing the Stability of AXIN2 mRNA.Oncology research · 2025Article
- Harnessing glycolysis in gastric cancer: molecular targets, therapeutic strategies, and clinical horizons.Frontiers in immunology · 2025Review
- Wnt/β-catenin signaling pathway: proteins' roles in osteoporosis and cancer diseases and the regulatory effects of natural compounds on osteoporosis.Molecular medicine (Cambridge, Mass.) · 2024Review
- The Emerging Role of LPA as an Oncometabolite.Cells · 2024Review
- Mn(III) Porphyrin, MnTnBuOE-2-PyPInternational journal of molecular sciences · 2023Article
- The Autotaxin-LPA Axis Emerges as a Novel Regulator of Smooth Muscle Cell Phenotypic Modulation during Intimal Hyperplasia.International journal of molecular sciences · 2023Article
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
Lysophosphatidic acid (LPA), a multifunctional endogenous phospholipid, plays a vital role in cellular homeostasis and the malignant behavior of cancer cells through G-protein-coupled receptors. However, the role of LPA in β-catenin-mediated gastric cancer is unknown. Here, we have noted the high expression of LPAR2 in human gastric cancer tissues, and that LPA treatment significantly increased the proliferation, migration, and invasion of human gastric cancer cells. Results from our biochemical experiments showed that an LPA exposure increased the expression of β-catenin and its nuclear localization, increased the phosphorylation of glycogen synthase kinase 3β (GSK-3β), decreased the expression of Axin2, and increased the expression of the target genes of the β-catenin signaling pathway. The LPA2 receptor (LPAR2) antagonist significantly reduced the LPA-induced nuclear localization of β-catenin, the primary signaling event. The knockdown of LPAR2 in the gastric cancer cell lines robustly reduced the LPA-induced β-catenin activity. An LPA exposure increased the ATP production by both oxidative phosphorylation and glycolysis, and this effect was abrogated with the addition of an LPAR2 antagonist and XAV393, which stabilizes the Axin and inhibits the β-catenin signaling pathway. Based on our findings, the possibility that LPA contributes to gastric cancer initiation and progression through the β-catenin signaling pathway as well as by the dysregulation of the energy metabolism via the LPAR2 receptor and Axin2, respectively, provides a novel insight into the mechanism of and possible therapeutic targets of gastric cancer.
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