ArticleProceedings of the National Academy of Sciences of the United States of America2019
FAM64A positively regulates STAT3 activity to promote Th17 differentiation and colitis-associated carcinogenesis.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 79 citations in OpenAlex.
- ABTB1, as an E3 ubiquitin ligase, suppresses Th17 cell differentiation and mitigates autoimmune inflammation by promoting STAT3 ubiquitination and degradation.Cellular & molecular immunology · 2026Article
- FAM64A Potentiates Bladder Carcinoma Tumorigenesis and Metastasis Through PI3K/mTORC2/AKT Pathway Activation.Cancers · 2026Article
- Targeting FAM64A: a promising strategy to halt liver cancer angiogenesis and enhance immunity.American journal of cancer research · 2026Article
- Yougui pills prevent ovariectomy-induced bone loss by suppressing Th17 response and IL-17/NF-κB pathway.Annals of medicine · 2025Article
- The glycolytic reaction PGAM restrains Th17 pathogenicity and Th17-dependent autoimmunity.Cell reports · 2025Article
- FAM64A silencing inhibits the proliferation, migration, invasion, and epithelial-mesenchymal transition in ovarian cancer cells via activating Hippo pathway.Discover oncology · 2025Article
- FAM64A contributes to ovarian cancer proliferation and metastasis by suppressing TWIST1 ubiquitination and degradation.Endocrine-related cancer · 2025Article
- Exosomes from Tregs mitigate lung damage caused by smoking via inhibiting inflammation and altering T lymphocyte subsets in COPD rats.BMC pulmonary medicine · 2025Article
- Oncogenic role and prognostic significance of PIMREG in melanoma.Translational cancer research · 2025Article
- FAM64A regulates the malignant phenotype and tumor microenvironment of non-small cell lung cancer by activating the JAK/STAT3/PDL1 axis.Journal of molecular histology · 2025Article
- Vitamin DCancers · 2024Article
- LDLR is an entry receptor for Crimean-Congo hemorrhagic fever virus.Cell research · 2024Article
- Intestinal Inflammation and Regeneration-Interdigitating Processes Controlled by Dietary Lipids in Inflammatory Bowel Disease.International journal of molecular sciences · 2024Review
- Th9 and Th17 Cells in Human Ulcerative Colitis-Associated Dysplastic Lesions.Clinical Medicine Insights. Oncology · 2024Article
- Selective IL-27 production by intestinal regulatory T cells permits gut-specific regulation of TNature immunology · 2023Article
- Article
- Explore the active ingredients and potential mechanisms of JianPi QingRe HuaYu Methods in the treatment of gastric inflammation-cancer transformation by network pharmacology and experimental validation.BMC complementary medicine and therapies · 2023Article
- Colitis-associated carcinogenesis: crosstalk between tumors, immune cells and gut microbiota.Cell & bioscience · 2023Review
- Factors impacting the benefits and pathogenicity of Th17 cells in the tumor microenvironment.Frontiers in immunology · 2023Review
- Article
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
STAT3 is a transcription factor that plays central roles in various physiological processes, including differentiation of Th cells. Its deregulation results in serious diseases, including inflammatory diseases and cancer. The mechanisms related to how STAT3 activity is regulated remain enigmatic. Here we show that overexpression of FAM64A potentiates IL-6-induced activation of STAT3 and expression of downstream target genes, whereas deficiency of FAM64A has the opposite effects. FAM64A interacts with STAT3 in the nucleus and regulates binding of STAT3 to the promoters of its target genes. Deficiency of Fam64a significantly impairs differentiation of Th17 but not Th1 or induced regulatory T cells (iTreg). In addition, Fam64a deficiency attenuates experimental autoimmune encephalomyelitis (EAE) and dextran sulfate sodium (DSS)-induced colitis, which is correlated with decreased differentiation of Th17 cells and production of proinflammatory cytokines. Furthermore, Fam64a deficiency suppresses azoxymethane (AOM)/DSS-induced colitis-associated cancer (CAC) in mice. These findings suggest that FAM64A regulates Th17 differentiation and colitis and inflammation-associated cancer by modulating transcriptional activity of STAT3.
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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.