ArticleOncogene2016
GPC5, a novel epigenetically silenced tumor suppressor, inhibits tumor growth by suppressing Wnt/β-catenin signaling in lung adenocarcinoma.
Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 82 citations in OpenAlex.
- Tumor promotion or suppression: Revisiting the role of EXT1 and Heparan sulfate.Histology and histopathology · 2026Review
- Whole-Genome Resequencing Identifies Candidate Genes for Tail Fat Deposition in Sheep.Animals : an open access journal from MDPI · 2025Article
- Review
- Development of a novel anti-human glypican 5 monoclonal antibody (GBiochemistry and biophysics reports · 2025Article
- Structural Features of Glypicans and their Impact on Wnt Signaling in Cancer.Proteoglycan research · 2025Article
- FAM210B activates STAT1/IRF9/IFIT3 axis by upregulating IFN-α/β expression to impede the progression of lung adenocarcinoma.Cell death & disease · 2025Article
- KCTD10 inhibits lung cancer metastasis and angiogenesis via ubiquitin-mediated β-catenin degradation.Frontiers in immunology · 2025Article
- Wnt/β-catenin signaling in the development and therapeutic resistance of non-small cell lung cancer.Journal of translational medicine · 2024Review
- Enhancing Genomic Prediction Accuracy for Body Conformation Traits in Korean Holstein Cattle.Animals : an open access journal from MDPI · 2024Article
- Exploring Heparan Sulfate Proteoglycans as Mediators of Human Mesenchymal Stem Cell Neurogenesis.Cellular and molecular neurobiology · 2024Review
- The Neural Progenitor Cell-Associated Transcription Factor FoxG1 Regulates Cardiac Epicardial Cell Proliferation.Stem cells international · 2024Article
- YTHDC1 as a tumor progression suppressor through modulating FSP1-dependent ferroptosis suppression in lung cancer.Cell death and differentiation · 2023Article
- A novel NET-related gene signature for predicting DLBCL prognosis.Journal of translational medicine · 2023Article
- WNT ligands in non-small cell lung cancer: from pathogenesis to clinical practice.Discover oncology · 2023Review
- RBM14 as a novel epigenetic-activated tumor oncogene is implicated in the reprogramming of glycolysis in lung cancer.World journal of surgical oncology · 2023Article
- LINC00669 promotes lung adenocarcinoma growth by stimulating the Wnt/β-catenin signaling pathway.Cancer medicine · 2023Article
- A topographic atlas defines developmental origins of cell heterogeneity in the human embryonic lung.Nature cell biology · 2023Article
- A potassium-chloride co-transporter promotes tumor progression and castration resistance of prostate cancer through mCell death & disease · 2023Article
- Why loss of Y? A pan-cancer genome analysis of tumors with loss of Y chromosome.Computational and structural biotechnology journal · 2023Article
- Bioinformatics and System Biology Approach to Reveal the Interaction Network and the Therapeutic Implications for Non-Small Cell Lung Cancer Patients With COVID-19.Frontiers in pharmacology · 2022Article
Corrections and comments
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Authors and funding
17 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glypican-5 (GPC5) is a member of the heparin sulfate proteoglycans. Previous studies of GPC5 in lung tumorigenesis showed conflicting results. In this study, we confirmed that GPC5 was downregulated in lung adenocarcinoma tissues compared with adjacent normal lung tissues. The low expression of GPC5 was significantly associated with poor outcome in lung adenocarcinoma. To understand the biological mechanism of the downregulation, we examined the promoter methylation status of GPC5 gene. We found that GPC5 was significantly hypermethylated in lung cancer tissues and lung cancer cell lines compared with normal lung tissues. The methylation level of GPC5 was negatively correlated with its transcriptional expression. De-methylation experiments further confirmed that the loss of GPC5 expression was regulated by its hypermethylation. Overexpression of GPC5 inhibited proliferation, migration and invasion of lung cancer cells in vitro, and repressed tumor growth in vivo, whereas knockdown of GPC5 was able to reverse the effect. Furthermore, we demonstrated that GPC5 could suppress the Wnt/β-catenin signaling by binding to Wnt3a at the cell surface, which mediated its function as a tumor suppressor. Overall, these findings demonstrate that GPC5 is a novel epigenetically silenced tumor suppressor, which inhibits tumor growth by suppressing Wnt/β-catenin signaling in lung adenocarcinoma. Our findings substantially expand our understanding about the role and the molecular mechanism of GPC5 in tumorigenesis of lung cancer.
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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.