ArticleJournal of cellular and molecular medicine2024
BUB1/KIF14 complex promotes anaplastic thyroid carcinoma progression by inducing chromosome instability.
Article in Journal of cellular and molecular medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 7 citations in OpenAlex.
- KIF14 in cancer biology: implications for diagnosis and therapy.Clinical & experimental metastasis · 2026Review
- BUB1 in cancer genetics and oncogenomics: from chromosomal instability to therapeutic vulnerabilities.Frontiers in genetics · 2026Review
- Validation of the important role and prognostic value of KIF14 in triple-negative breast cancer.Cancer biology & therapy · 2025Article
- Post-translational modifications in anaplastic thyroid carcinoma: biological mechanisms and therapeutic potential.Cancer cell international · 2025Review
- FTO Promotes Hepatocellular Carcinoma Progression by Mediating m6A Modification of BUB1 and Targeting TGF-βR1 to Activate the TGF-β Signaling Pathway.Journal of clinical and translational hepatology · 2025Article
- KIF14 plays a role in the regulation of the cell cycle and has implications for prognosis in clear cell renal cell carcinoma.BMC urology · 2025Article
- Expression and clinical significance of BUB1 in esophageal cancer.American journal of translational research · 2025Article
- PLXNB1/SEMA4D signals mediate interactions between malignant epithelial and immune cells to promote colorectal cancer liver metastasis.Journal of cellular and molecular medicine · 2024Article
- BUB1/KIF14 complex promotes anaplastic thyroid carcinoma progression by inducing chromosome instability.Journal of cellular and molecular medicine · 2024Article
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
Abstract
Chromosome instability (CIN) is a common contributor driving the formation and progression of anaplastic thyroid cancer (ATC), but its mechanism remains unclear. The BUB1 mitotic checkpoint serine/threonine kinase (BUB1) is responsible for the alignment of mitotic chromosomes, which has not been thoroughly studied in ATC. Our research demonstrated that BUB1 was remarkably upregulated and closely related to worse progression-free survival. Knockdown of BUB1 attenuated cell viability, invasion, migration and induced cell cycle arrests, whereas overexpression of BUB1 promoted the cell cycle progression of papillary thyroid cancer cells. BUB1 knockdown remarkably repressed tumour growth and tumour formation of nude mice with ATC xenografts and suppressed tumour metastasis in a zebrafish xenograft model. Inhibition of BUB1 by its inhibitor BAY-1816032 also exhibited considerable anti-tumour activity. Further studies showed that enforced expression of BUB1 evoked CIN in ATC cells. BUB1 induced CIN through phosphorylation of KIF14 at serine1292 (Ser
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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.