ArticleFrontiers in immunology2016
Human C1q Induces Apoptosis in an Ovarian Cancer Cell Line
Article in Frontiers in immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 47 citations in OpenAlex.
- C1qAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- KCC2 inhibition and neuronal hyperexcitability promote extrinsic apoptosis dependent upon C1q.Frontiers in molecular neuroscience · 2025Article
- Adipocyte-derived CXCL10 in obesity promotes the migration and invasion of ovarian cancer cells.Journal of ovarian research · 2024Article
- Causal relationship between complementFrontiers in genetics · 2024Article
- Absolute Quantification of Pan-Cancer Plasma Proteomes Reveals Unique Signature in Multiple Myeloma.Cancers · 2023Article
- Bax Contributes to Retinal Ganglion Cell Dendritic Degeneration During Glaucoma.Molecular neurobiology · 2022Article
- Detection of Complement C1q B Chain Overexpression and Its Latent Molecular Mechanisms in Cervical Cancer Tissues Using Multiple Methods.International journal of genomics · 2022Article
- Prognostic and immune-related value of complement C1Q (C1QA, C1QB, and C1QC) in skin cutaneous melanoma.Frontiers in genetics · 2022Article
- Review
- Prognostic Implications of the Complement Protein C1Q and Its Correlation with Immune Infiltrates in Osteosarcoma.OncoTargets and therapy · 2021Article
- Targeting the Complement Pathway in Malignant Glioma Microenvironments.Frontiers in cell and developmental biology · 2021Review
- Modulation of the Complement System by Neoplastic Disease of the Central Nervous System.Frontiers in immunology · 2021Review
- Complement System: Promoter or Suppressor of Cancer Progression?Antibodies (Basel, Switzerland) · 2020Review
- Alcohol Increases Exosome Release from Microglia to Promote Complement C1q-Induced Cellular Death of Proopiomelanocortin Neurons in the Hypothalamus in a Rat Model of Fetal Alcohol Spectrum Disorders.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Serum proteomics analysis of feline mammary carcinoma based on label-free and PRM techniques.Journal of veterinary science · 2020Article
- Complement and human T cell metabolism: Location, location, location.Immunological reviews · 2020Review
- Identification ofFrontiers in oncology · 2020Article
- Globular C1q Receptor (gC1qR/p32/HABP1) Suppresses the Tumor-Inhibiting Role of C1q and Promotes Tumor Proliferation in 1q21-Amplified Multiple Myeloma.Frontiers in immunology · 2020Article
- Context-dependent roles of complement in cancer.Nature reviews. Cancer · 2019Review
- Cigarette smoke-induced reduction of C1q promotes emphysema.JCI insight · 2019Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Complement protein C1q is the first recognition subcomponent of the complement classical pathway that plays a vital role in the clearance of immune complexes, pathogens, and apoptotic cells. C1q also has a homeostatic role involving immune and non-immune cells; these functions not necessarily involve complement activation. Recently, C1q has been shown to be expressed locally in the microenvironment of a range of human malignant tumors, where it can promote cancer cell adhesion, migration, and proliferation, without involving complement activation. C1q has been shown to be present in the ascitic fluid formed during ovarian cancers. In this study, we have examined the effects of human C1q and its globular domain on an ovarian cancer cell line, SKOV3. We show that C1q and the recombinant globular head modules induce apoptosis in SKOV3 cells in a time-dependent manner. C1q expression was not detectable in the SKOV3 cells. Exogenous treatment with C1q and globular head modules at the concentration of 10 µg/ml induced apoptosis in approximately 55% cells, as revealed by immunofluorescence microscopy and FACS. The qPCR and caspase analysis suggested that C1q and globular head modules activated tumor necrosis factor (TNF)-α and upregulated Fas. The genes of mammalian target of rapamycin (mTOR), RICTOR, and RAPTOR survival pathways, which are often overexpressed in majority of the cancers, were significantly downregulated within few hours of the treatment of SKOV3 cells with C1q and globular head modules. In conclusion, C1q,
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