ArticleThe Journal of clinical investigation2012
FAM83A confers EGFR-TKI resistance in breast cancer cells and in mice.
Article in The Journal of clinical investigation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers.
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Who cites it
101 citing papers in PubMed, 170 citations in OpenAlex.
- Hypomethylation of FAM83A in lung adenocarcinoma mirrors an epigenetic signature of airway cell differentiation states.Discover oncology · 2026Article
- M2 macrophage-derived extracellular vesicles induce EMT-like transcriptional reprogramming in colorectal cancer cells via upregulation of FAM83A.Scientific reports · 2026Article
- A putative prognostic model for lung adenocarcinoma based on crotonylation-related genes by bioinformatics and experimental verification.Frontiers in cell and developmental biology · 2026Article
- FAM83A is a prognostic biomarker for lung squamous cell carcinoma and correlated with immunoregulation.Scientific reports · 2025Article
- FAM83A may serve as a potential prognostic indicator for stomach adenocarcinoma.Translational cancer research · 2025Article
- Metabolic Reprogramming-Related Genes in Lung Adenocarcinoma: Identification and Prognostic Model Construction.World journal of oncology · 2025Article
- The complex role and molecular mechanism of family with sequence similarity genes in cancer: a comprehensive review.Discover oncology · 2025Review
- Immunogenic shift of arginine metabolism triggers systemic metabolic and immunological reprogramming to suppress HER2 + breast cancer.Cancer & metabolism · 2025Article
- Oviductal extracellular matrix hydrogels enhance in vitro culture of rabbit embryos and reduce deficiencies during assisted reproductive technologies.Scientific reports · 2024Article
- Zebrafish reveal new roles for Fam83f in hatching and the DNA damage-mediated autophagic response.Open biology · 2024Article
- Promotion of stem cell-like phenotype of lung adenocarcinoma by FAM83A via stabilization of ErbB2.Cell death & disease · 2024Article
- Diagnostic value of immune-related biomarker FAM83A in differentiating malignant from benign pleural effusion in lung adenocarcinoma.Discover oncology · 2024Article
- Article
- Unveiling Alterations of Epigenetic Modifications and Chromatin Architecture Leading to Lipid Metabolic Reprogramming during the Evolutionary Trastuzumab Adaptation of HER2-Positive Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- High-fat diet promotes prostate cancer metastasis via RPS27.Cancer & metabolism · 2024Article
- Identification of a novel immunogenic death-associated model for predicting the immune microenvironment in lung adenocarcinoma from single-cell and Bulk transcriptomes.Journal of Cancer · 2024Article
- FAM83A promotes the progression and metastasis of human pancreatic neuroendocrine tumors by inducing the epithelial-mesenchymal transition via the PI3K/AKT and ERK pathways.Journal of endocrinological investigation · 2023Article
- Regulation of early diagnosis and prognostic markers of lung adenocarcinoma in immunity and hypoxia.Scientific reports · 2023Article
- B-lymphoid tyrosine kinase-mediated FAM83A phosphorylation elevates pancreatic tumorigenesis through interacting with β-catenin.Signal transduction and targeted therapy · 2023Article
- ncRNA-mediated upregulation ofFrontiers in endocrinology · 2023Article
41 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Breast cancers commonly become resistant to EGFR-tyrosine kinase inhibitors (EGFR-TKIs); however, the mechanisms of this resistance remain largely unknown. We hypothesized that resistance may originate, at least in part, from molecular alterations that activate signaling downstream of EGFR. Using a screen to measure reversion of malignant cells into phenotypically nonmalignant cells in 3D gels, we identified FAM83A as a candidate cancer-associated gene capable of conferring resistance to EGFR-TKIs. FAM83A overexpression in cancer cells increased proliferation and invasion and imparted EGFR-TKI resistance both in cultured cells and in animals. Tumor cells that survived EGFR-TKI treatment in vivo had upregulated FAM83A levels. Additionally, FAM83A overexpression dramatically increased the number and size of transformed foci in cultured cells and anchorage-independent growth in soft agar. Conversely, FAM83A depletion in cancer cells caused reversion of the malignant phenotype, delayed tumor growth in mice, and rendered cells more sensitive to EGFR-TKI. Analyses of published clinical data revealed a correlation between high FAM83A expression and breast cancer patients' poor prognosis. We found that FAM83A interacted with and caused phosphorylation of c-RAF and PI3K p85, upstream of MAPK and downstream of EGFR. These data provide an additional mechanism by which tumor cells can become EGFR-TKI resistant.
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