ArticleOncogene2014
Hyperactivation of EGFR and downstream effector phospholipase D1 by oncogenic FAM83B.
Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
31 citing papers in PubMed, 40 citations in OpenAlex.
- Evaluating the Effectiveness of Tyrosine Kinase Inhibitors on EGFR Mutations In Vitro.International journal of molecular sciences · 2025Article
- Development and Evaluation of Indole-Based Phospholipase D Inhibitors for Lung Cancer Immunotherapy.Journal of medicinal chemistry · 2025Article
- Construction of a Prognostic Model for Cervical Cancer Related to lncRNA Based on Differential Co-expression Network and Functional Study of Key Gene EGFR-AS1.Journal of Cancer · 2025Article
- Article
- Genetic characterization of Tibetan pigs adapted to high altitude under natural selection based on a large whole-genome dataset.Scientific reports · 2024Article
- The receptor protein tyrosine phosphatase PTPRK promotes intestinal repair and catalysis-independent tumour suppression.Journal of cell science · 2024Article
- EGFR TKI resistance in lung cancer cells using RNA sequencing and analytical bioinformatics tools.Journal of biomolecular structure & dynamics · 2023Article
- Involvement of FAM83 Family Proteins in the Development of Solid Tumors: An Update Review.Journal of Cancer · 2023Review
- Structural insights into PA3488-mediated inactivation of Pseudomonas aeruginosa PldA.Nature communications · 2022Article
- FAM83B is involved in thyroid cancer cell differentiation and migration.Scientific reports · 2022Article
- LncRNA FAM83A-AS1 facilitates tumor proliferation and the migration via the HIF-1α/ glycolysis axis in lung adenocarcinoma.International journal of biological sciences · 2022Article
- The phospholipase D inhibitor FIPI potently blocks EGF-induced calcium signaling in human breast cancer cells.Cell communication and signaling : CCS · 2021Article
- FAM83A and FAM83A-AS1 both play oncogenic roles in lung adenocarcinoma.Oncology letters · 2021Article
- Differential genomics and transcriptomics between tyrosine kinase inhibitor-sensitive and -resistant BCR-ABL-dependent chronic myeloid leukemia.Oncotarget · 2018Article
- The FAM83 family of proteins: from pseudo-PLDs to anchors for CK1 isoforms.Biochemical Society transactions · 2018Review
- Family with sequence similarity 83, member B is a predictor of poor prognosis and a potential therapeutic target for lung adenocarcinoma expressing wild-type epidermal growth factor receptor.Oncology letters · 2018Article
- PLD1 overexpression promotes invasion and migration and function as a risk factor for Chinese glioma patients.Oncotarget · 2017Article
- Family with sequence similarity 13C (FAM13C) overexpression is an independent prognostic marker in prostate cancer.Oncotarget · 2017Article
- Targeting phospholipase D in cancer, infection and neurodegenerative disorders.Nature reviews. Drug discovery · 2017Review
- Multiple across-strain and within-strain QTLs suggest highly complex genetic architecture for hypoxia tolerance in channel catfish.Molecular genetics and genomics : MGG · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Despite the progress made in targeted anticancer therapies in recent years, challenges remain. The identification of new potential targets will ensure that the arsenal of cancer therapies continues to expand. FAM83B was recently discovered in a forward genetic screen for novel oncogenes that drive human mammary epithelial cell (HMEC) transformation. We report here that elevated FAM83B expression increases Phospholipase D (PLD) activity, and that suppression of PLD1 activity prevents FAM83B-mediated transformation. The increased PLD activity is engaged by hyperactivation of epidermal growth factor receptor (EGFR), which is regulated by an interaction involving FAM83B and EGFR. Preventing the FAM83B/EGFR interaction by site-directed mutation of lysine 230 of FAM83B suppressed PLD activity and MAPK signaling. Furthermore, ablation of FAM83B expression from breast cancer cells inhibited EGFR phosphorylation and suppressed cell proliferation. We propose that understanding the mechanism of FAM83B-mediated transformation will provide a foundation for future therapies aimed at targeting its function as an intermediary in EGFR, MAPK and mTOR activation.
Indexed as
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What OpenQuestion holds
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.