ArticleCell death discovery2024
KIFC1 depends on TRIM37-mediated ubiquitination of PLK4 to promote centrosome amplification in endometrial cancer.
Article in Cell death discovery, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Targeting the KIFC1-SRSF3-PKM Axis Suppresses Cervical Cancer Glycolysis and Enhances Radiosensitivity.Journal of cellular and molecular medicine · 2026Article
- Indium (III) chloride inhibits testicular Leydig cell proliferation by disrupting centrosome copy numbers.Molecular medicine reports · 2026Article
- Targeting KIFC1 to disrupt centrosome clustering and trigger anaphase catastrophe in small-cell lung cancer.JCI insight · 2026Article
- ALKBH5/IGF2BP1-mediated mCell biology and toxicology · 2026Article
- KIFC1 is Associated With Sarcomatoid Differentiation, Immune Response, and a Poor Prognosis in Clear Cell Renal Cell Carcinoma.Cancer medicine · 2026Article
- TRIM37 recognizes a bipartite degron to ubiquitinate centrosome substrates.bioRxiv : the preprint server for biology · 2025Article
- Review
- Polo-like kinase 4 (PLK4) as a therapeutic target in breast cancer.Carcinogenesis · 2025Review
- KIFC1 Overexpression Promotes Pancreatic Carcinoma Progression via Stabilising BUB1B.Journal of cellular and molecular medicine · 2025Article
- Analysis of the differential transcriptome expression profiles during prenatal muscle tissue development in Diqing Tibetan pigs.Frontiers in veterinary science · 2025Article
Corrections and comments
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Authors and funding
6 authors.
Funding
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Abstract
Endometrial cancer (EC), as one of the most common cancers, severely threatens female reproductive health. Our previous study has shown that Kinesin family member C1 (KIFC1) played crucial roles in the progression of EC. In addition, abnormal centrosome amplification, which was reported to be partially regulated by KIFC1, usually occurred in different cancers. However, whether KIFC1 promoted EC through centrosome amplification and the potential mechanism remain to be revealed. The present study demonstrated that overexpressed KIFC1, which exhibited a worse prognosis, had a positive correlation with an increased number of centrosomes in human EC samples. In addition, KIFC1 overexpression in EC cells prompted centrosome amplification, chromosomal instability, and cell cycle progression. Moreover, we demonstrated that KIFC1 inhibited E3 ubiquitin-protein ligase TRIM37 to maintain the stability of PLK4 by reducing its ubiquitination degradation, and finally promoting centrosome amplification and EC progression in vitro. Finally, the contributing role of KIFC1 and the inhibitory effect of TRIM37 on EC development and metastasis was verified in a nude mouse xenograft model. Our study elucidated that KIFC1 depends on TRIM37-mediated reduced ubiquitination degradation of PLK4 to promote centrosome amplification and EC progression, thus providing a potential prognostic marker and promising therapeutic target for EC in the future.
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