ArticleCommunications biology2021
Depletion of kinesin motor KIF20A to target cell fate control suppresses medulloblastoma tumour growth.
Article in Communications biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- Targeting mitotic kinesin KIF20A: A differentiation-based therapeutic strategy for glioblastoma stem/progenitor cells.Stem cell reports · 2026Article
- Integrated Bioinformatics Analysis Identifies NCAPG2 as an Immune-Related Prognostic Biomarker in Breast Cancer.World journal of oncology · 2026Article
- Decoding the Role of Kinesin Superfamily Proteins in Glioma Progression.Journal of molecular neuroscience : MN · 2025Review
- Knockdown of CENPF induces cell cycle arrest and inhibits epithelial‑mesenchymal transition progression in glioma.Oncology letters · 2025Article
- A Four-Gene Panel for the Prediction of Prognosis and Immune Cell Enrichment in Gliomas.Molecular biotechnology · 2024Article
- Advancing Cancer Therapy: The Role of KIF20A as a Target for Inhibitor Development and Immunotherapy.Cancers · 2024Review
- Targeting Wnt signaling for improved glioma immunotherapy.Frontiers in immunology · 2024Article
- Delineating the glioblastoma stemness by genes involved in cytoskeletal rearrangements and metabolic alterations.World journal of stem cells · 2023Review
- Review
- Identification of PBK as a hub gene and potential therapeutic target for medulloblastoma.Oncology reports · 2022Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
During mammalian brain development, neural progenitor cells proliferate extensively but can ensure the production of correct numbers of various types of mature cells by balancing symmetric proliferative versus asymmetric differentiative cell divisions. This process of cell fate determination may be harnessed for developing cancer therapy. Here, we test this idea by targeting KIF20A, a mitotic kinesin crucial for the control of cell division modes, in a genetic model of medulloblastoma (MB) and human MB cells. Inducible Kif20a knockout in both normal and MB-initiating granule neuron progenitors (GNPs) causes early cell cycle exit and precocious neuronal differentiation without causing cytokinesis failure and suppresses the development of Sonic Hedgehog (SHH)-activated MB. Inducible KIF20A knockdown in human MB cells inhibits proliferation both in cultures and in growing tumors. Our results indicate that targeting the fate specification process of nascent daughter cells presents a novel avenue for developing anti-proliferation treatment for malignant brain tumors.
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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.