ArticleCell death & disease2023
PLK1 and AURKB phosphorylate survivin differentially to affect proliferation in racially distinct triple-negative breast cancer.
Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 49 citations in OpenAlex.
- AURKB drives aggressive phenotype and clinicopathological progression in cholangiocarcinoma.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Article
- A Multi-Omics Framework Reveals Tumor Heterogeneity and Predicts Therapeutic Targets in Renal Cell Carcinoma.International journal of molecular sciences · 2026Article
- Biomarker, treatment patterns, and survival differences in metastatic triple-negative breast cancer by race in the United States.NPJ breast cancer · 2026Article
- Multifunctional fluorescent carbon dots with synergistic-mechanism targeted mitochondria and Fe³⁺ detection.Mikrochimica acta · 2026Article
- Pseudolaric acid B promotes lung cancer cells ferroptosis depending on JNK/ERK-mediated upregulation of survivin.Scientific reports · 2026Article
- The effect of PARP and PLK1 dual inhibition on the expression of important protein signaling pathways, DNA damage, and molecular docking scores against MCF-7 and MDA-MB-231 breast cancer cell lines.Irish journal of medical science · 2026Article
- Bioinformatics analysis identifies AURKB as a prognostic biomarker across multiple human cancers.Discover oncology · 2026Article
- Discovery of Small Molecule Inhibitors against Polo-Like Kinase 1 Targeting Breast Cancer.Anti-cancer agents in medicinal chemistry · 2026Article
- PLK1 overexpression as a dual-role biomarker and therapeutic vulnerability in pulmonary adenocarcinoma.PeerJ · 2026Article
- Computational and experimental discovery of peptide inhibitors targeting survivin for therapeutic potential in cancer.Scientific reports · 2025Article
- Histone lactylation-boosted AURKB facilitates colorectal cancer progression by inhibiting HNRNPM-mediated PSAT1 mRNA degradation.Journal of experimental & clinical cancer research : CR · 2025Article
- ECM characterization and 3D bioprinted models of NSCLC for investigating stiffness-dependent tumor behavior and drug response.Materials today. Bio · 2025Article
- Article
- Transcriptome Analysis of Canine Histiocytic Sarcoma Tumors and Cell Lines Reveals Multiple Targets for Therapy.Cancers · 2025Article
- Proteomic profiling identifies upregulation of aurora kinases causing resistance to taxane-type chemotherapy in triple negative breast cancer.Scientific reports · 2025Article
- Development and validation of a novel sodium-overload related genes signature for prognostic prediction in breast cancer: integrating bioinformatics and experimental approaches.Frontiers in immunology · 2025Article
- Advances in hydrogel-based materials for breast cancer bone metastasis: from targeted drug delivery to bone microenvironment remodeling.Frontiers in pharmacology · 2025Review
- Article
- Functional and structural impacts of oncogenic missense variants on human polo-like kinase 1 protein.Frontiers in bioinformatics · 2025Article
- [High expression of AURKB promotes malignant phenotype of osteosarcoma cells by activating nuclear factor-κB signalingNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024Article
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
Protein diversity due to alternative mRNA splicing or post-translational modifications (PTMs) plays a vital role in various cellular functions. The mitotic kinases polo-like kinase 1 (PLK1) and Aurora B (AURKB) phosphorylate survivin, an inhibitor of apoptosis (IAP) family member, thereby regulating cell proliferation. PLK1, AURKB, and survivin are overexpressed in triple-negative breast cancer (TNBC), an aggressive breast cancer subtype. TNBC is associated with high proliferative capacity, high rates of distant metastasis, and treatment resistance. The proliferation-promoting protein survivin and its activating kinases, PLK1 and AURKB, are overexpressed in TNBC. In this study, we investigated the role of survivin phosphorylation in racial disparities in TNBC cell proliferation. Analysis of TCGA TNBC data revealed higher expression levels of PLK1 (P = 0.026) and AURKB (P = 0.045) in African Americans (AAs; n = 41) than in European Americans (EAs; n = 86). In contrast, no significant racial differences in survivin mRNA or protein levels were observed. AA TNBC cells exhibited higher p-survivin levels than EA TNBC cells. Survivin silencing using small interfering RNAs significantly attenuated cell proliferation and cell cycle progression in AA TNBC cells, but not in EA TNBC cells. In addition, PLK1 and AURKB inhibition with volasertib and barasertib significantly inhibited the growth of AA TNBC xenografts, but not of EA TNBC tumors. These data suggest that inhibition of PLK1 and AURKB suppresses cell proliferation and tumor growth, specifically in AA TNBC. These findings suggest that targeting survivin phosphorylation may be a viable therapeutic option for AA patients with TNBC.
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Registered trials
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