ArticleScientific reports2016
14-3-3γ Prevents Centrosome Amplification and Neoplastic Progression.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 34 citations in OpenAlex.
- Proteomics analysis reveals progesterone receptor induced mitochondria-mediated apoptosis in breast cancer cells.Scientific reports · 2025Article
- 14-3-3ε inhibits premature centriole disengagement by inhibiting the activity of Plk1 and separase.Journal of cell science · 2025Article
- Article
- Role of the YWHAG gene mutations in Developmental and Epileptic Encephalopathy.Frontiers in neuroscience · 2025Review
- 14-3-3ε conditional knockout mice exhibit defects in the development of the epidermis.FEBS letters · 2024Article
- Systematic identification of post-transcriptional regulatory modules.Nature communications · 2024Article
- Up-Regulated MISP Is Associated With Poor Prognosis and Immune Infiltration in Pancreatic Ductal Adenocarcinoma.Frontiers in oncology · 2022Article
- Article
- Centrosome amplification: a quantifiable cancer cell trait with prognostic value in solid malignancies.Cancer metastasis reviews · 2021Review
- NPM1 Biology in Myeloid Neoplasia.Current hematologic malignancy reports · 2020Review
- Differential Subcellular Distribution and Translocation of Seven 14-3-3 Isoforms in Response to EGF and During the Cell Cycle.International journal of molecular sciences · 2020Article
- New insights into the biology of acute myeloid leukemia with mutated NPM1.International journal of hematology · 2019Review
- 14-3-3 proteins mediate the localization of Centrin2 to centrosome.Journal of biosciences · 2019Article
- Resting cells rely on the DNA helicase component MCM2 to build cilia.Nucleic acids research · 2019Article
- Overcome cancer drug resistance by targeting epigenetic modifications of centrosome.Cancer drug resistance (Alhambra, Calif.) · 2019Review
- Deep-proteome mapping of WM-266-4 human metastatic melanoma cells: From oncogenic addiction to druggable targets.PloS one · 2017Article
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
More than 80% of malignant tumors show centrosome amplification and clustering. Centrosome amplification results from aberrations in the centrosome duplication cycle, which is strictly coordinated with DNA-replication-cycle. However, the relationship between cell-cycle regulators and centrosome duplicating factors is not well understood. This report demonstrates that 14-3-3γ localizes to the centrosome and 14-3-3γ loss leads to centrosome amplification. Loss of 14-3-3γ results in the phosphorylation of NPM1 at Thr-199, causing early centriole disjunction and centrosome hyper-duplication. The centrosome amplification led to aneuploidy and increased tumor formation in mice. Importantly, an increase in passage of the 14-3-3γ-knockdown cells led to an increase in the number of cells containing clustered centrosomes leading to the generation of pseudo-bipolar spindles. The increase in pseudo-bipolar spindles was reversed and an increase in the number of multi-polar spindles was observed upon expression of a constitutively active 14-3-3-binding-defective-mutant of cdc25C (S216A) in the 14-3-3γ knockdown cells. The increase in multi-polar spindle formation was associated with decreased cell viability and a decrease in tumor growth. Our findings uncover the molecular basis of regulation of centrosome duplication by 14-3-3γ and inhibition of tumor growth by premature activation of the mitotic program and the disruption of centrosome clustering.
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