ArticleCancer discovery2013
Cancer-Specific requirement for BUB1B/BUBR1 in human brain tumor isolates and genetically transformed cells.
Article in Cancer discovery, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers, 1 of them a synthesis that pooled it.
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Who cites it
65 citing papers in PubMed, 1 synthesis or guideline pooled it, 97 citations in OpenAlex.
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- KAT5 regulates neurodevelopmental states associated with G0-like populations in glioblastoma.Nature communications · 2025Article
- BubR1 and SIRT2: Insights into aneuploidy, aging, and cancer.Seminars in cancer biology · 2024Review
- Centromeres in cancer: Unraveling the link between chromosomal instability and tumorigenesis.Medical oncology (Northwood, London, England) · 2024Review
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- Novel Tetrazole Derivatives Targeting Tubulin Endowed with Antiproliferative Activity against Glioblastoma Cells.International journal of molecular sciences · 2023Article
- Improving Localized Radiotherapy for Glioblastoma via Small Molecule Inhibition of KIF11.Cancers · 2023Article
- Target-Based Anticancer Indole Derivatives for the Development of Anti-Glioblastoma Agents.Molecules (Basel, Switzerland) · 2023Review
- Characteristic Analysis of Featured Genes Associated with Cholangiocarcinoma Progression.Biomedicines · 2023Article
- The "Superoncogene" Myc at the Crossroad between Metabolism and Gene Expression in Glioblastoma Multiforme.International journal of molecular sciences · 2023Review
- Identification of Differentially Methylated Genes Associated with Clear Cell Renal Cell Carcinoma and Their Prognostic Values.Journal of environmental and public health · 2023Article
- Clinical value and potential mechanisms of BUB1B up-regulation in nasopharyngeal carcinoma.BMC medical genomics · 2022Article
- Hyper-active RAS/MAPK introduces cancer-specific mitotic vulnerabilities.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Bioinformatic identification of differentially expressed genes associated with hepatocellular carcinoma prognosis.Medicine · 2022Article
- Aberrant Expression of BUB1B Contributes to the Progression of Thyroid Carcinoma and Predicts Poor Outcomes for Patients.Journal of Cancer · 2022Article
- BUB1 drives the occurrence and development of bladder cancer by mediating the STAT3 signaling pathway.Journal of experimental & clinical cancer research : CR · 2021Article
5 more citing papers are in PubMed but not listed here.
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Authors and funding
18 authors at 8 institutions in 3 countries.
Funding
Abstract
unlabelledTo identify new candidate therapeutic targets for glioblastoma multiforme, we combined functional genetics and glioblastoma network modeling to identify kinases required for the growth of patient-derived brain tumor-initiating cells (BTIC) but that are dispensable to proliferating human neural stem cells (NSC). This approach yielded BUB1B/BUBR1, a critical mitotic spindle checkpoint player, as the top-scoring glioblastoma lethal kinase. Knockdown of BUB1B inhibited expansion of BTIC isolates, both in vitro and in vivo, without affecting proliferation of NSCs or astrocytes. Mechanistic studies revealed that BUB1B's GLE2p-binding sequence (GLEBS) domain activity is required to suppress lethal kinetochore-microtubule (KT-MT) attachment defects in glioblastoma isolates and genetically transformed cells with altered sister KT dynamics, which likely favor KT-MT instability. These results indicate that glioblastoma tumors have an added requirement for BUB1B to suppress lethal consequences of altered KT function and further suggest that sister KT measurements may predict cancer-specific sensitivity to BUB1B inhibition and perhaps other mitotic targets that affect KT-MT stability. SIGNIFICANCE: Currently, no effective therapies are available for glioblastoma, the most frequent and aggressive brain tumor. Our results suggest that targeting the GLEBS domain activity of BUB1B may provide a therapeutic window for glioblastoma, as the GLEBS domain is nonessential in untransformed cells. Moreover, the results further suggest that sister KT distances at metaphase may predict sensitivity to anticancer therapeutics targeting KT function.
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