ArticleScientific reports2018
Complement C1q stimulates the progression of hepatocellular tumor through the activation of discoidin domain receptor 1.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 48 citations in OpenAlex.
- Complement system in tumor growth and metastases.British journal of cancer · 2026Review
- C1q drives neural stem cell quiescence by regulating cell cycle and metabolism through BAI1.Nature communications · 2025Article
- Stage-specific TRIM10 expression regulates erythroid maturation.EMBO reports · 2025Article
- C1qAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Article
- Emerging strategies and translational advancements of DDR1 in oncology.Discover oncology · 2025Review
- Research progress on the roles of complement in liver injury.World journal of hepatology · 2025Review
- Non-canonical extracellular complement pathways and the complosome paradigm in cancer: a scoping review.Frontiers in immunology · 2025Article
- Role of DDR1 in Regulating MMPs in External Root Resorption.International journal of molecular sciences · 2024Article
- Organelle phenotyping and multi-dimensional microscopy identify C1q as a novel regulator of microglial function.Journal of neurochemistry · 2024Article
- 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
- Immune proteins C1q and CD47 may contribute to aberrant microglia-mediated synapse loss in the aging monkey brain that is associated with cognitive impairment.GeroScience · 2024Article
- Epigenetic regulation of complement C1Q gene expression.Frontiers in immunology · 2024Article
- Exploring the Cellular and Molecular Mechanism of Discoidin Domain Receptors (DDR1 and DDR2) in Bone Formation, Regeneration, and Its Associated Disease Conditions.International journal of molecular sciences · 2023Review
- Focusing on discoidin domain receptors in premalignant and malignant liver diseases.Frontiers in oncology · 2023Review
- Complement C1QC as a potential prognostic marker and therapeutic target in colon carcinoma based on single-cell RNA sequencing and immunohistochemical analysis.Bosnian journal of basic medical sciences · 2022Article
- Understanding the contextual functions of C1q and LAIR-1 and their applications.Experimental & molecular medicine · 2022Review
- Discoidin domain receptor 1 promotes hepatocellular carcinoma progression through modulation of SLC1A5 and the mTORC1 signaling pathway.Cellular oncology (Dordrecht, Netherlands) · 2022Article
- High complement protein C1q levels in pulmonary fibrosis and non-small cell lung cancer associated with poor prognosis.BMC cancer · 2022Article
- An update on the role of complement in hepatocellular carcinoma.Frontiers in immunology · 2022Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
C1q is known to perform several functions in addition to the role it plays in complement activation. C1q contains a collagen-like portion and DDR1 (discoidin domain receptor 1) is a well-known collagen receptor. Accordingly, we hypothesized C1q might be a novel ligand of DDR1. This study shows for the first time C1q directly induces the activation and upregulation of DDR1, and that this leads to enhanced migration and invasion of HepG2 cells. In addition, C1q was found to induce the activations of mitogen-activated protein kinases (MAPKs) and phosphoinositide 3-kinase (PI3K)/Akt signaling, and to increase the expressions of matrix metalloproteinases (MMP2 and 9). Our results reveal a relationship between C1q and DDR1 and suggest C1q-induced DDR1 activation signaling may be involved in the progression of hepatocellular carcinoma.
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Registered trials
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.