ArticleCancers2019
Upregulation of Complement Factor H by SOCS-1/3⁻STAT4 in Lung Cancer.
Article in Cancers, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
19 citing papers in PubMed, 33 citations in OpenAlex.
- KIAA1199 aggravates sepsis-induced lung injury by promoting complement activation.Communications biology · 2026Article
- Complement factor H in cancer biology: intracellular functions, tumor-host interactions, and systemic context.Frontiers in immunology · 2026Review
- Identification of PD-L1-related biomarkers for selecting gastric adenocarcinoma patients for PD-1/PD-L1 inhibitor therapy.Discover oncology · 2025Article
- Complement Factor H Promotes the Growth of Lung Adenocarcinoma Cells through the JAK2/STAT3 Signaling Pathway.Current cancer drug targets · 2025Article
- A transcriptomic analysis of dental pulp stem cell senescence in vitro.Biomedical engineering online · 2024Article
- Complement factor H in molecular regulation of angiogenesis.Medical review (2021) · 2024Review
- The human factor H protein family - an update.Frontiers in immunology · 2024Review
- STAT4 gene polymorphisms in human diseases.Frontiers in immunology · 2024Review
- Identification of Key Prognostic Alternative Splicing Events of Costimulatory Molecule-Related Genes in Colon Cancer.Combinatorial chemistry & high throughput screening · 2024Article
- Analysis of complement system and its related factors in Alzheimer's disease.BMC neurology · 2023Article
- Downregulation of complement factor H attenuates the stemness of MDA‑MB‑231 breast cancer cells via modulation of the ERK and p38 signaling pathways.Oncology letters · 2023Article
- Assessment of STAT4 Variants and Risk of Hepatocellular Carcinoma in Latin Americans and Europeans.Cancers · 2023Article
- Impact of STAT Proteins in Tumor Progress and Therapy Resistance in Advanced and Metastasized Prostate Cancer.Cancers · 2021Review
- Xanthatin synergizes with cisplatin to suppress homologous recombination through JAK2/STAT4/BARD1 axis in human NSCLC cells.Journal of cellular and molecular medicine · 2021Article
- Targeting the Complement Pathway in Malignant Glioma Microenvironments.Frontiers in cell and developmental biology · 2021Review
- Sex Disparities of Genomic Determinants in Response to Immune Checkpoint Inhibitors in Melanoma.Frontiers in immunology · 2021Article
- Tumour extracellular vesicle-derived Complement Factor H promotes tumorigenesis and metastasis by inhibiting complement-dependent cytotoxicity of tumour cells.Journal of extracellular vesicles · 2020Article
- In-Depth Mapping of the UrinaryCancers · 2020Article
- How Does Complement Affect Hematological Malignancies: From Basic Mechanisms to Clinical Application.Frontiers in immunology · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Complement factor H (CFH) is a fluid phase regulator of complement proteins and functions to prevent complement attack and immune surveillance. CFH is known to inactivate therapeutic antibody-dependent complement-mediated cellular cytotoxicity. We found that CFH was highly expressed in human lung cancer cells and tissues. To investigate mechanisms of CFH upregulation, we searched for a CFH transcription factor and its regulatory factors. First, signal transducer and activator of transcription 4 (STAT4) expression patterns coincided with CFH expression patterns in lung cancer tissues. Knockdown of STAT4 led to decreased CFH secretion from lung cancer cells. STAT4 bound directly to the CFH promoter, as demonstrated by luciferase reporter assay, electrophoretic mobility shift assay (EMSA), and chromatin immunoprecipitation (ChIP) assay, suggesting that STAT4 is a transcription factor for CFH. In addition, a low level of suppressors of cytokine signaling (SOCS)-1/3, a Janus kinase (JAK) inhibitor, was observed in lung cancer cells and its transfection decreased CFH protein levels and promoter activity. Unexpectedly, the low level of SOCS-1/3 was not due to epigenetic silencing. Instead, differential methylation was found on the regulatory region of STAT4 between normal and lung cancer cells. In conclusion, our results demonstrated that CFH is upregulated by constitutive activation of STAT4, which is accounted for by SOCS silencing in lung cancer cells.
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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.