ArticleJournal of clinical medicine2019
KIFC1 Inhibitor CW069 Induces Apoptosis and Reverses Resistance to Docetaxel in Prostate Cancer.
Article in Journal of clinical medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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
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Who cites it
32 citing papers in PubMed, 53 citations in OpenAlex.
- Kinesins in Cancer Drug Resistance: Mechanisms, Therapeutic Targeting, and Translational Potential.Cancers · 2026Review
- ALDH+ Anaplastic Thyroid Cancer Cells Show Vulnerability to a Pharmacologic Inducer of Centrosome Declustering.Cancer research communications · 2026Article
- Targeting KIFC1 to disrupt centrosome clustering and trigger anaphase catastrophe in small-cell lung cancer.JCI insight · 2026Article
- KIFC1 Overexpression Promotes Pancreatic Carcinoma Progression via Stabilising BUB1B.Journal of cellular and molecular medicine · 2025Article
- Pan-Cancer Analysis Shows that KIFC2 is a Potential Prognostic and Immunotherapeutic Biomarker for Multiple Cancer Types Including Bladder Cancer.Molecular biotechnology · 2025Article
- Two cancer cell lines utilize Myosin 10 and the kinesin HSET differentially to maintain mitotic spindle bipolarity.PloS one · 2025Article
- Article
- Development of a prostate cancer biochemical recurrence risk signature using machine learning and motor protein-related genes.PloS one · 2025Article
- The role of kinesin superfamily proteins in hepatocellular carcinoma.Medical oncology (Northwood, London, England) · 2024Review
- Kinesin Facilitates Phenotypic Targeting of Therapeutic Resistance in Advanced Prostate Cancer.Molecular cancer research : MCR · 2024Article
- Surviving the Storm: The Role of Poly- and Depolyploidization in Tissues and Tumors.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Review
- The Eμ-Ret mouse is a novel model of hyperdiploid B-cell acute lymphoblastic leukemia.Leukemia · 2024Article
- High Expression of KIFC1 in Glioma Correlates with Poor Prognosis.Journal of Korean Neurosurgical Society · 2024Article
- The role of kinesin family members in hepatobiliary carcinomas: from bench to bedside.Biomarker research · 2024Review
- IQ Motif Containing GTPase-Activating Protein 3 Is Associated with Cancer Stemness and Survival in Pancreatic Ductal Adenocarcinoma.Pathobiology : journal of immunopathology, molecular and cellular biology · 2024Article
- Article
- Emerging roles of centrosome cohesion.Open biology · 2022Review
- Terminally differentiated osteoclasts organize centrosomes into large clusters for microtubule nucleation and bone resorption.Molecular biology of the cell · 2022Article
- Circ_0004087 interaction with SND1 promotes docetaxel resistance in prostate cancer by boosting the mitosis error correction mechanism.Journal of experimental & clinical cancer research : CR · 2022Article
- Circular RNAs in prostate cancer: Biogenesis,biological functions, and clinical significance.Molecular therapy. Nucleic acids · 2021Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Kinesin family member C1 (KIFC1) is a minus end-directed motor protein that plays an essential role in centrosome clustering. Previously, we reported that KIFC1 is involved in cancer progression in prostate cancer (PCa). We designed this study to assess the involvement of KIFC1 in docetaxel (DTX) resistance in PCa and examined the effect of KIFC1 on DTX resistance. We also analyzed the possible role of a KIFC1 inhibitor (CW069) in PCa. We used DTX-resistant PCa cell lines in DU145 and C4-2 cells to analyze the effect of KIFC1 on DTX resistance in PCa. Western blotting showed that KIFC1 expression was higher in the DTX-resistant cell lines than in the parental cell lines. Downregulation of KIFC1 re-sensitized the DTX-resistant cell lines to DTX treatment. CW069 treatment suppressed cell viability in both parental and DTX-resistant cell lines. DTX alone had little effect on cell viability in the DTX-resistant cells. However, the combination of DTX and CW069 significantly reduced cell viability in the DTX-resistant cells, indicating that CW069 re-sensitized the DTX-resistant cell lines to DTX treatment. These results suggest that a combination of CW069 and DTX could be a potential strategy to overcome DTX resistance.
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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 Socratic graph.