ArticleOncogene2021
GPC5 suppresses lung cancer progression and metastasis via intracellular CTDSP1/AhR/ARNT signaling axis and extracellular exosome secretion.
Article in Oncogene, 2021. 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, 22 citations in OpenAlex.
- Dual evidence reveals the therapeutic efficacy of exosome-delivered miR-124-3p in spinal cord injury via a novel CTDSP1/WNT/β-catenin mechanism.Spinal cord · 2026Article
- Development of a novel anti-human glypican 5 monoclonal antibody (GBiochemistry and biophysics reports · 2025Article
- A rare germline mutation reverses the suppressive effect ofFrontiers in genetics · 2025Article
- miR-26b Targets CEP135 Gene to Regulate Nasopharyngeal Carcinoma Proliferation and Migration by NF-κB Pathway.Molecular biotechnology · 2023Article
- Phosphorylation of AHR by PLK1 promotes metastasis of LUAD via DIO2-TH signaling.PLoS genetics · 2023Article
- Review
- Aryl hydrocarbon receptor-kynurenine axis promotes oncogenic activity in BCP-ALL.Cell biology and toxicology · 2023Article
- Research Trends in C-Terminal Domain Nuclear Envelope Phosphatase 1.Life (Basel, Switzerland) · 2023Review
- Exosome-Mediated Therapeutic Strategies for Management of Solid and Hematological Malignancies.Cells · 2022Review
- The critical role of STAT3 in biogenesis of tumor-derived exosomes with potency of inducing cancer cachexia in vitro and in vivo.Oncogene · 2022Article
- Identification of microRNA editing sites in three subtypes of leukemia.Frontiers in molecular biosciences · 2022Article
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lung cancer is the leading cause of cancer-related death worldwide. Glypican-5 (GPC5) is a member of heparan sulfate proteoglycans, and its biological importance in initiation and progression of lung cancer remains controversial. In the present study, we revealed that GPC5 transcriptionally enhanced the expression of CTDSP1 (miR-26b host gene) via AhR-ARNT pathway, and such up-regulation of CTDSP1 intracellularly contributed to the inhibited proliferation of lung cancer cells. Moreover, exosomes derived from GPC5-overexpressing human lung cancer cells (GPC5-OE-derived exosomes) had an extracellular repressive effect on human lymphatic endothelial cells (hLECs), leading to decreased tube formation and migration. Comparison between GPC5-WT- and GPC5-OE-derived exosomes showed that miR-26b (embedded within introns of CTDSP1 gene) was significantly up-regulated in GPC5-OE-derived exosomes and critical to the influence on hLECs. On the mechanism, we demonstrated that miR-26b transferred into hLECs directly targeted to PTK2 3'-UTR and led to PTK2 down-regulation, resulting in defects in tube formation and migration of hLECs. By uncovering the regulation network among GPC5, miR-26b, miR-26b host gene (CTDSP1), and target gene (PTK2), our findings demonstrated that GPC5 functioned as a tumor suppressor in human lung cancer.
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