ArticleNature communications2015
Loss of KLF14 triggers centrosome amplification and tumorigenesis.
Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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Who cites it
61 citing papers in PubMed, 116 citations in OpenAlex.
- Centriolar satellites regulatebioRxiv : the preprint server for biology · 2026Article
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- Genetic Variations inMolecular syndromology · 2025Article
- Polo-like kinase 4 (PLK4) as a therapeutic target in breast cancer.Carcinogenesis · 2025Review
- Genetic variations and functions of KLF14 in gene expression and metabolic disease development.Journal of applied genetics · 2025Review
- Review
- KLF14 inhibits tumor progression via FOSL1 in glioma.Biochemistry and biophysics reports · 2025Article
- Targeting KIFC1 Promotes Senescence in Soft Tissue Sarcoma via FXR1-Dependent Regulation of MAD2L1 mRNA Stability.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- KLF14 directly downregulates the expression of GPX4 to exert antitumor effects by promoting ferroptosis in cervical cancer.Journal of translational medicine · 2024Article
- Lactylated Apolipoprotein C-II Induces Immunotherapy Resistance by Promoting Extracellular Lipolysis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Exploring the impact of circRNAs on cancer glycolysis: Insights into tumor progression and therapeutic strategies.Non-coding RNA research · 2024Review
- Chromatin Remodeling in Patient-Derived Colorectal Cancer Models.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Molecular mechanism of WWP1-mediated ubiquitination modification affecting proliferation and invasion/migration of liver cancer cells.The Kaohsiung journal of medical sciences · 2024Article
- Nudt21-mediated alternative polyadenylation of MZT1 3'UTR contributes to pancreatic cancer progression.iScience · 2024Article
- Repression of latent NF-κB enhancers by PDX1 regulates β cell functional heterogeneity.Cell metabolism · 2024Article
- Lactylation of METTL16 promotes cuproptosis via mNature communications · 2023Article
- Downregulation of Krüppel-like factor 14 accelerated cellular senescence and aging.Aging cell · 2023Article
- Article
- Biochemical Activation and Regulatory Functions of Trans-Regulatory KLF14 and Its Association with Genetic Polymorphisms.Metabolites · 2023Review
- KLF14 regulates the growth of hepatocellular carcinoma cells via its modulation of iron homeostasis through the repression of iron-responsive element-binding protein 2.Journal of experimental & clinical cancer research : CR · 2023Article
1 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
19 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Centrosome amplification is frequent in cancer, but the underlying mechanisms remain unclear. Here we report that disruption of the Kruppel-like factor 14 (KLF14) gene in mice causes centrosome amplification, aneuploidy and spontaneous tumorigenesis. Molecularly, KLF14 functions as a transcriptional repressor of Plk4, a polo-like kinase whose overexpression induces centrosome overduplication. Transient knockdown of KLF14 is sufficient to induce Plk4-directed centrosome amplification. Clinically, KLF14 transcription is significantly downregulated, whereas Plk4 transcription is upregulated in multiple types of cancers, and there exists an inverse correlation between KLF14 and Plk4 protein expression in human breast and colon cancers. Moreover, KLF14 depletion promotes AOM/DSS-induced colon tumorigenesis. Our findings reveal that KLF14 reduction serves as a mechanism leading to centrosome amplification and tumorigenesis. On the other hand, forced expression of KLF14 leads to mitotic catastrophe. Collectively, our findings identify KLF14 as a tumour suppressor and highlight its potential as biomarker and therapeutic target for cancer.
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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.