ArticleOncogene2005
Krüppel-like factor 4 prevents centrosome amplification following gamma-irradiation-induced DNA damage.
Article in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
56 citing papers in PubMed, 88 citations in OpenAlex.
- Krüppel-like Factor 4-Deficient Cells Are Sensitive to Etoposide-Induced DNA Damage.Current issues in molecular biology · 2025Article
- Inhibiting centrosome clustering reduces cystogenesis and improves kidney function in autosomal dominant polycystic kidney disease.JCI insight · 2024Article
- Integrated whole transcriptome profiling revealed a convoluted circular RNA-based competing endogenous RNAs regulatory network in colorectal cancer.Scientific reports · 2024Article
- New insights into KLFs and SOXs in cancer pathogenesis, stemness, and therapy.Seminars in cancer biology · 2023Review
- Review
- Proteins That Read DNA Methylation.Advances in experimental medicine and biology · 2022Article
- KLF4 transactivates TRIM29 expression and modulates keratin network.Biochemistry and biophysics reports · 2021Article
- Centrosome amplification: a quantifiable cancer cell trait with prognostic value in solid malignancies.Cancer metastasis reviews · 2021Review
- Characterization of increased mucus production of HT29-MTX-E12 cells grown under Semi-Wet interface with Mechanical Stimulation.PloS one · 2021Article
- New insight into the significance of KLF4 PARylation in genome stability, carcinogenesis, and therapy.EMBO molecular medicine · 2020Article
- Genome-wide association study identifies genetic susceptibility loci and pathways of radiation-induced acute oral mucositis.Journal of translational medicine · 2020Article
- MicroRNA-7 Regulates Migration and Chemoresistance in Non-Hodgkin Lymphoma Cells Through Regulation of KLF4 and YY1.Frontiers in oncology · 2020Article
- Regulation of Krüppel-Like Factor 4 (KLF4) expression through the transcription factor Yin-Yang 1 (YY1) in non-Hodgkin B-cell lymphoma.Oncotarget · 2019Article
- DNA Methylation Readers and Cancer: Mechanistic and Therapeutic Applications.Frontiers in oncology · 2019Review
- Krüppel-like factor 4 is a negative regulator of STAT3-induced glomerular epithelial cell proliferation.JCI insight · 2018Article
- FBXO32 suppresses breast cancer tumorigenesis through targeting KLF4 to proteasomal degradation.Oncogene · 2017Article
- Inactivation of KLF4 promotes T-cell acute lymphoblastic leukemia and activates the MAP2K7 pathway.Leukemia · 2017Article
- SP and KLF Transcription Factors in Digestive Physiology and Diseases.Gastroenterology · 2017Review
- Review
- Aging and the Krüppel-like factors.Trends in cell & molecular biology · 2017Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Centrosome duplication is a carefully controlled process in the cell cycle. Previous studies indicate that the tumor suppressor, p53, regulates centrosome duplication. Here, we present evidence for the involvement of the mammalian Krüppel-like transcription factor, KLF4, in preventing centrosome amplification following DNA damage caused by gamma-irradiation. The colon cancer cell line HCT116, which contains wild-type p53 alleles (HCT116 p53+/+), displayed stable centrosome numbers following gamma-irradiation. In contrast, HCT116 cells null for the p53 alleles (HCT116 p53-/-) exhibited centrosome amplification after irradiation. In the latter cell line, KLF4 was not activated following gamma-irradiation due to the absence of p53. However, centrosome amplification could be suppressed in irradiated HCT116 p53-/- cells by conditional induction of exogenous KLF4. Conversely, in a HCT116 p53+/+ cell line stably transfected with small hairpin RNA (shRNA) designed to specifically inhibit KLF4, gamma-irradiation induced centrosome amplification. In these cells, the inability of KLF4 to become activated in response to DNA damage was directly associated with an increase in cyclin E level and Cdk2 activity, both essential for regulating centrosome duplication. Cotransfection experiments showed that KLF4 overexpression suppressed the promoter activity of the cyclin E gene. The results of this study demonstrated that KLF4 is both necessary and sufficient in preventing centrosome amplification following gamma-radiation-induced DNA damage and does so by transcriptionally suppressing cyclin E expression.
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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.