ArticleBritish journal of cancer2006
FADD phosphorylation is critical for cell cycle regulation in breast cancer cells.
Article in British journal of cancer, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 50 citations in OpenAlex.
- Targeting casein kinase 1α-mediated FADD phosphorylation restores sensitivity in select CDK4/6 inhibitor-resistant breast cancer models.The Journal of clinical investigation · 2026Article
- Synergistic combinatorial anticancer potential of Tamoxifen with Naringin and Diosmetin in MCF-7 breast cancer cells and their liposomal delivery.Scientific reports · 2026Article
- Establishment and validation of a recurrent prediction model for glioma: extrinsic apoptotic molecules FADD and CASP8 are closely associated with glioma recurrence.BMC immunology · 2025Article
- FADD Activation in Hepatocellular Carcinoma Potentiates CD8+ T-cell Responses and Sensitizes to Immune Checkpoint Inhibitors.Cancer research · 2025Article
- Identification of autoantibodies as potential non-invasive biomarkers for intrahepatic cholangiocarcinoma.Scientific reports · 2024Article
- FADD regulates adipose inflammation, adipogenesis, and adipocyte survival.Cell death discovery · 2024Article
- FADD phosphorylation contributes to development of renal fibrosis by accelerating epithelial-mesenchymal transition.Cell cycle (Georgetown, Tex.) · 2023Article
- FADD as a key molecular player in cancer progression.Molecular medicine (Cambridge, Mass.) · 2022Review
- Metabolomic Identification of Anticancer Metabolites of Australian Propolis and Proteomic Elucidation of Its Synergistic Mechanisms with Doxorubicin in the MCF7 Cells.International journal of molecular sciences · 2021Article
- HIPK3 Inhibition by Exosomal hsa-miR-101-3p Is Related to Metabolic Reprogramming in Colorectal Cancer.Frontiers in oncology · 2021Article
- Article
- FADD Phosphorylation Modulates Blood Glucose Levels by Decreasing the Expression of Insulin-Degrading Enzyme.Molecules and cells · 2020Article
- Review
- Concordance between somatic copy number loss and down-regulated expression: A pan-cancer study of cancer predisposition genes.Scientific reports · 2016Article
- FADD is a key regulator of lipid metabolism.EMBO molecular medicine · 2016Article
- Increased Expression of Phosphorylated FADD in Anaplastic Large Cell and Other T-Cell Lymphomas.Biomarker insights · 2014Article
- Role of Fas-associated death domain-containing protein (FADD) phosphorylation in regulating glucose homeostasis: from proteomic discovery to physiological validation.Molecular & cellular proteomics : MCP · 2013Article
- Regulation of protein kinase C inactivation by Fas-associated protein with death domain.The Journal of biological chemistry · 2012Article
- Methylseleninic acid enhances paclitaxel efficacy for the treatment of triple-negative breast cancer.PloS one · 2012Article
- Expression of serine 194-phosphorylated Fas-associated death domain protein correlates with proliferation in B-cell non-Hodgkin lymphomas.Human pathology · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Anti-oestrogen therapy is effective for control of hormone receptor-positive breast cancers, although the detailed molecular mechanisms, including signal transduction, remain unclear. We demonstrated here that long-term tamoxifen treatment causes G2/M cell cycle arrest through c-jun N-terminal kinase (JNK) activation, which is dependent on phosphorylation of Fas-associated death domain-containing protein (FADD) at 194 serine in an oestrogen (ER) receptor-positive breast cancer cell line, MCF-7. Expression of a dominant negative mutant form of MKK7, a kinase upstream of JNK, or mutant FADD (S194A) in MCF-7 cells suppressed the cytotoxicity of long-term tamoxifen treatment. Of great interest, similar signallings could be evoked by paclitaxel, even in an ER-negative cell line, MDA-MB-231. In addition, immunohistochemical analysis using human breast cancer specimens showed a close correlation between phosphorylated JNK and FADD expression, both being significantly reduced in cases with metastatic potential. We conclude that JNK-mediated phosphorylation of FADD plays an important role in the negative regulation of cell growth and metastasis, independent of the ER status of a breast cancer, so that JNK/FADD signals might be promising targets for cancer therapy.
Indexed as
Identifiers
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.