Ask about this productRelated genes to: NEDD9 antibody
- Gene:
- NEDD9 NIH gene
- Name:
- neural precursor cell expressed, developmentally down-regulated 9
- Previous symbol:
- -
- Synonyms:
- HEF1, CAS-L, CASS2
- Chromosome:
- 6p24.2
- Locus Type:
- gene with protein product
- Date approved:
- 1994-01-21
- Date modifiied:
- 2015-08-25
Related products to: NEDD9 antibody
Related articles to: NEDD9 antibody
- Excessive centrosome activation is detrimental to normal cells by hampering bipolar-spindle formation during mitosis and inducing cell death. In the highly aggressive anaplastic thyroid cancer (ATC), cells expressing the ALDH+ stem-cell trait are enriched in supernumerary centrosomes and tolerate centrosome amplification, which offers these cells a growth advantage. Our earlier work characterized the chromosomal instability within this cell population, which was due to dysfunctional centrosomes manifesting as a deficiency in pericentriolar material. Here, we report a novel 2-(4-morpholinoanilino-6-[(2-exo-norbornyl) amino)-purine (MEAP) that preferentially restores centrosome microtubule-nucleation activity in centrosome-deficient ALDH+ ATC cells. Exposure of these cells to MEAP induced pericentriolar accumulation and microtubule-nucleation activity of supernumerary centrosomes, resulting in spindle multipolarity. Consequently, MEAP was capable of preferentially eliminating ALDH+ ATC cell population, thus reducing cell spherogenesis and self-renewal capacity. In a preclinical ATC mouse model, MEAP preferentially eliminated ALDH+ cell clusters, increased the rate of spindle multipolarity, decreased chromosomal instability, and generated a robust antitumor response. Lastly, we identified that the selective activity of MEAP in ALDH+ cells involved the modulation of NEDD9-STAT3 signaling. Together, these findings support the potential of targeting centrosome amplification as an alternative therapeutic approach for aggressive ALDH+ cancers failing first line therapeutics. - Source: PubMed
Publication date: 2026/04/24
Yu Henry GuanghaoBijian KrikorSu JieWernic DominikAlaoui-Jamali Moulay A - During cancer metastasis, tumor cells survive in circulation by acquiring resistance to anoikis. Restoring vulnerability of cancer cells to anoikis can impair metastatic colonization, minimize treatment resistance, and tumor recurrence in patients. A compelling body of evidence has identified strategies for the development of effective inhibitors that can block survival pathways such as FAK, PI3K/AKT, MAPK and integrin signaling to prevent prostate cancer cells from leaving the primary tumor/site and/or to impair their colonization at secondary sites. Transcriptomic profiling recently identified anoikis-centered genes, including CDKN1A, NEDD9, CFL1, and JAM2, that may have potential prognostic value in prostate cancer progression and may also contribute to the emergence of therapeutic resistance to antiandrogens and taxane chemotherapy. Direct cytoskeletal remodeling by cofilin, a transforming growth factor-β (TGF-β) effector is linked to phenotypic plasticity changes. NEDD9 causes cytoskeletal dynamics through signaling pathways and it is correlated with tumor aggressiveness. CDKN1A affects cell cycle regulation, and JAM2 influences cell adhesion. This review interrogates the current evidence in the literature on the cellular drivers of anoikis resistance, intersecting with phenotypic plasticity in the prostate tumor microenvironment, toward determination of the underlying molecular mechanisms that can be exploited at the translational level for therapeutic applications. The identification and subsequent validation of novel anoikis-resistance based signatures can be of potential value as predictive markers of therapy resistance and tumor recurrence in patients with advanced prostate cancer. - Source: PubMed
Kouspou MariaZhu AlecMartires LaurenTewari Ashutosh KMehrazin RezaKyprianou Natasha - The microRNA (miR) cluster miR-143/145 represents a well-characterized tumor-suppressive regulatory system with a multifaceted role in prostate cancer. Both miRs are consistently downregulated during disease progression, and their loss is associated with enhanced proliferation, invasion, epithelial–mesenchymal transition, and metastatic competence. Mechanistically, the cluster modulates Rat Sarcoma Viral Oncogene Homolog (RAS)-Mitogen Activated Protein Kinase (MAPK) signaling via Kirsten Rat Sarcoma Viral Oncogene Homolog (KRAS) and Extracellular Signal-Regulated Kinase 5 (ERK5), Tumor Protein p53 (p53)-dependent growth control through MYC Proto-Oncogene, Basic Helix-Loop-Helix Transcription Factor (c-MYC) repression, apoptosis via B-Cell Lymphoma 2 Interacting Protein 3 (BNIP3), and cytoskeleton-associated motility factors including Fascin Actin-Bundling Protein 1 (FSCN1), Human Enhancer of Filamentation 1/ Neural Precursor Cell Expressed, Developmentally Down-Regulated Protein 9 (HEF1/NEDD9), Golgi Membrane Protein 1 (GOLM1), and Fibronectin Type III Domain Containing 3B (FNDC3B). Downregulation is mainly driven by p53 dysfunction, promoter methylation, and RAS-dependent transcriptional repression. A defining feature is pronounced cell-type specificity, with tumor-suppressive effects in epithelial cells and context-dependent pro-angiogenic functions in stromal compartments, with direct translational relevance. Clinically, miR-143/145 contribute to multimarker diagnostic signatures, while reduced miR-145 correlates with adverse pathology and biochemical recurrence. Preclinical replacement strategies reduce tumor growth and enhance docetaxel sensitivity, yet context-dependent effects necessitate cell type-specific delivery. Overall, the cluster represents a central regulator with diagnostic, prognostic, and therapeutic potential requiring prospective validation. - Source: PubMed
Publication date: 2026/04/11
Stope Matthias BErb Holger H H - Pulmonary arterial hypertension (PAH) is an underrecognized cardiovascular complication of Graves' disease (GD). The role of thyroid autoimmunity and neural precursor-cell-expressed developmentally downregulated 9 (NEDD9), a profibrotic protein, in GD with PAH remains unclear. This study evaluated the prevalence, predictors of PAH, role of thyroid autoimmunity and NEDD9, and reversibility with carbimazole in newly diagnosed GD and PAH. - Source: PubMed
Publication date: 2026/02/27
Sahu Pradosh KPadala Ravi KDash Deepak KPatro DebasishSatpathy ChhabiDash Bandana - Pseudomyogenic hemangioendothelioma (PMHE) is a rare, low-grade vascular neoplasm that presents cutaneously as erythematous papules or nodules. Diagnosis is challenging, as PMHE can mimic more common benign dermatological conditions and shares histological similarities with high-grade tumors, particularly epithelioid sarcoma. We present the case of an 18-year-old male with a two-year history of a tender, indurated, dark brown subcutaneous plaque on his right upper thigh with histopathologic features consistent with PMHE. Genetic testing revealed a novel gene fusion, NEDD9::FOSB, which has not previously been reported in the literature, adding to the current genetic understanding of PMHE, and warrants further exploration as a potential therapeutic target. - Source: PubMed
Publication date: 2026/03/26
Sampath SuchitaD'Angelo CathleenShenoy ArchanaRubrecht AshlieAldrink Jennifer HFernandez Faith Esteban