ArticleFrontiers in immunology2023
Complement protein C1q stimulates hyaluronic acid degradation
Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 8 citations in OpenAlex.
- The Complosome: An Emerging Intracellular Complement Network in Cancer Development and Therapy.International journal of molecular sciences · 2026Review
- Hyaluronidase treatment is associated with increased cytokine levels and reduced peritoneal neutrophil accumulation during LPS-induced inflammation.Frontiers in pharmacology · 2026Article
- Hyaluronan: An Architect and Integrator for Cancer and Neural Diseases.International journal of molecular sciences · 2025Review
- Non-canonical extracellular complement pathways and the complosome paradigm in cancer: a scoping review.Frontiers in immunology · 2025Article
- Increasing serum complement component 1q is associated with worse prognosis in advanced non-small cell lung cancer treated with immune checkpoint inhibitors: a single-center, retrospective study.Journal of thoracic disease · 2024Article
- Epigenetic regulation of complement C1Q gene expression.Frontiers in immunology · 2024Article
- Causal relationship between complementFrontiers in genetics · 2024Article
- TMEM2: A New Dimension in Hyaluronan Biology.Proteoglycan researchArticle
Corrections and comments
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Authors and funding
15 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Complement component C1q can act as a pro-tumorigenic factor in the tumor microenvironment (TME). The TME in malignant pleural mesothelioma (MPM) is rich in C1q and hyaluronic acid (HA), whose interaction enhances adhesion, migration and proliferation of malignant cells. HA-bound C1q is also capable of modulating HA synthesis. Thus, we investigated whether HA-C1q interaction would affect HA degradation, analyzing the main degradation enzymes, hyaluronidase (HYAL)1 and HYAL2, and a C1q receptor candidate. We first proceeded with the characterization of HYALs in MPM cells, especially HYAL2, since bioinformatics survival analysis revealed that higher
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Registered trials
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