ArticleOncotarget2015
HSET overexpression fuels tumor progression via centrosome clustering-independent mechanisms in breast cancer patients.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.
What it found
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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
50 citing papers in PubMed, 1 synthesis or guideline pooled it, 81 citations in OpenAlex.
- Prognostic and clinicopathological significance of kinesin family member C1 in various cancers: A meta-analysis.Medicine · 2019Pooled it
- KIFC1 engages RUNX2/TGF-β signaling to promote lung cancer bone metastasis via disrupting bone homeostasis.Oncogene · 2026Article
- Cell Cycle-Specific Regulation of Centrosome Clustering Dynamics in Cancer Cells by the Multifunctional Kinesin HSET.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Microtubule regulation in cancer cells.Frontiers in cell and developmental biology · 2025Article
- Article
- Two cancer cell lines utilize Myosin 10 and the kinesin HSET differentially to maintain mitotic spindle bipolarity.PloS one · 2025Article
- Kinesins regulate the heterogeneity in centrosome clustering after whole-genome duplication.Life science alliance · 2024Article
- Review
- Article
- Kinesin Family Member C1 (KIFC1/HSET) Underlies Aggressive Disease in Androgen Receptor-Low and Basal-Like Triple-Negative Breast Cancers.International journal of molecular sciences · 2023Article
- Identification of KIFC1 as an independent prognostic marker in renal clear cell carcinoma correlates with tumor proliferation and immune infiltration.Scientific reports · 2023Article
- Centrosome linker diversity and its function in centrosome clustering and mitotic spindle formation.The EMBO journal · 2023Article
- Targeting TACC3 represents a novel vulnerability in highly aggressive breast cancers with centrosome amplification.Cell death and differentiation · 2023Article
- Role of motor proteins in human cancers.Saudi journal of biological sciences · 2022Review
- Racial Disparity in Quadruple Negative Breast Cancer: Aggressive Biology and Potential Therapeutic Targeting and Prevention.Cancers · 2022Review
- Keep Calm and Carry on with Extra Centrosomes.Cancers · 2022Review
- Kinesin Family Member C1 (KIFC1/HSET): A Potential Actionable Biomarker of Early Stage Breast Tumorigenesis and Progression of High-Risk Lesions.Journal of personalized medicine · 2021Review
- Modeling reveals cortical dynein-dependent fluctuations in bipolar spindle length.Biophysical journal · 2021Article
- Computational Drug Repositioning Identifies Statins as Modifiers of Prognostic Genetic Expression Signatures and Metastatic Behavior in Melanoma.The Journal of investigative dermatology · 2021Article
- High KIFC1 expression is associated with poor prognosis in prostate cancer.Medical oncology (Northwood, London, England) · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 5 institutions in 1 country.
Funding
Abstract
Human breast tumors harbor supernumerary centrosomes in almost 80% of tumor cells. Although amplified centrosomes compromise cell viability via multipolar spindles resulting in death-inducing aneuploidy, cancer cells tend to cluster extra centrosomes during mitosis. As a result cancer cells display bipolar spindle phenotypes to maintain a tolerable level of aneuploidy, an edge to their survival. HSET/KifC1, a kinesin-like minus-end directed microtubule motor has recently found fame as a crucial centrosome clustering molecule. Here we show that HSET promotes tumor progression via mechanisms independent of centrosome clustering. We found that HSET is overexpressed in breast carcinomas wherein nuclear HSET accumulation correlated with histological grade and predicted poor progression-free and overall survival. In addition, deregulated HSET protein expression was associated with gene amplification and/or translocation. Our data provide compelling evidence that HSET overexpression is pro-proliferative, promotes clonogenic-survival and enhances cell-cycle kinetics through G2 and M-phases. Importantly, HSET co-immunoprecipitates with survivin, and its overexpression protects survivin from proteasome-mediated degradation, resulting in its increased steady-state levels. We provide the first evidence of centrosome clustering-independent activities of HSET that fuel tumor progression and firmly establish that HSET can serve both as a potential prognostic biomarker and as a valuable cancer-selective therapeutic target.
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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.