ArticleMolecular cancer2023
BID expression determines the apoptotic fate of cancer cells after abrogation of the spindle assembly checkpoint by AURKB or TTK inhibitors.
Article in Molecular cancer, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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17 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.
- Polymorphisms within autophagy-related genes as susceptibility biomarkers for pancreatic cancer: A meta-analysis of three large European cohorts and functional characterization.International journal of cancer · 2025Pooled it
- Targeting the DDX3/PAF1 axis enhances chemotherapy efficacy in pancreatic ductal adenocarcinoma.Cancer letters · 2026Article
- Article
- Bioinformatics analysis identifies AURKB as a prognostic biomarker across multiple human cancers.Discover oncology · 2026Article
- Aurora kinase B phosphorylates ZBP1 to drive PANoptosis following treatment with PARP and ATR inhibitors combination.Nature communications · 2025Article
- Oncotransformation in Bhas 42 Cell Transformation Assay by Typical Non-Genotoxic Carcinogens, PFOA and PFOS, and Time-Course Transcriptome Analysis.Biomolecules · 2025Article
- LncRNA938/ TAF9/TTK axis promotes EMT and serves as a therapeutic target in hepatoblastoma.Journal of translational medicine · 2025Article
- A new era in cancer therapy: targeting the Proteasome-Bcl-2 axis.Journal of experimental & clinical cancer research : CR · 2025Review
- Aurora kinases signaling in cancer: from molecular perception to targeted therapies.Molecular cancer · 2025Review
- Integrated machine learning survival framework develops a prognostic model based on macrophage-related genes and programmed cell death signatures in a multi-sample Kidney renal clear cell carcinoma.Cell biology and toxicology · 2025Article
- Aurora B inhibition induces hyper-polyploidy and loss of long-term proliferative potential in RB and p53 defective cells.Cell death & disease · 2025Article
- Integrating traditional omics and AI-driven approaches for discovery and validation of novel MicroRNA biomarkers and therapeutic targets in thyroid cancer.Frontiers in pharmacology · 2025Article
- Cell cycle proteins: Linking the cell cycle to tumors.Oncology research · 2025Review
- Unveiling BID: a key biomarker in apoptosis post-intracerebral hemorrhage.Frontiers in neurology · 2025Article
- Caspase-2 kills cells with extra centrosomes.Science advances · 2024Article
- Amplified centrosomes-more than just a threat.EMBO reports · 2024Review
- Canonical and Noncanonical Functions of the BH3 Domain Protein Bid in Apoptosis, Oncogenesis, Cancer Therapeutics, and Aging.Cancers · 2024Review
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Authors and funding
29 authors at 9 institutions in 6 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDrugs targeting the spindle assembly checkpoint (SAC), such as inhibitors of Aurora kinase B (AURKB) and dual specific protein kinase TTK, are in different stages of clinical development. However, cell response to SAC abrogation is poorly understood and there are no markers for patient selection.
methodsA panel of 53 tumor cell lines of different origins was used. The effects of drugs were analyzed by MTT and flow cytometry. Copy number status was determined by FISH and Q-PCR; mRNA expression by nCounter and RT-Q-PCR and protein expression by Western blotting. CRISPR-Cas9 technology was used for gene knock-out (KO) and a doxycycline-inducible pTRIPZ vector for ectopic expression. Finally, in vivo experiments were performed by implanting cultured cells or fragments of tumors into immunodeficient mice.
resultsTumor cells and patient-derived xenografts (PDXs) sensitive to AURKB and TTK inhibitors consistently showed high expression levels of BH3-interacting domain death agonist (BID), while cell lines and PDXs with low BID were uniformly resistant. Gene silencing rendered BID-overexpressing cells insensitive to SAC abrogation while ectopic BID expression in BID-low cells significantly increased sensitivity. SAC abrogation induced activation of CASP-2, leading to cleavage of CASP-3 and extensive cell death only in presence of high levels of BID. Finally, a prevalence study revealed high BID mRNA in 6% of human solid tumors.
conclusionsThe fate of tumor cells after SAC abrogation is driven by an AURKB/ CASP-2 signaling mechanism, regulated by BID levels. Our results pave the way to clinically explore SAC-targeting drugs in tumors with high BID expression.
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