Cyclin K as a direct transcriptional target of the p53 tumor suppressor.
Cyclin K, a newly recognized member of the "transcription" cyclin family, may play a dual role by regulating CDK and transcription. Using cDNA microarray technology, we found that cyclin K mRNA was dramatically increased in U373MG, a glioblastoma cell line deficient in wild-type p53, in the presence of exogenous p53. An electrophoretic mobility-shift assay showed that a potential p53- binding site (p53BS) in intron 1 of the cyclin K gene could indeed bind to p53 protein. Moreover, a heterologous reporter assay revealed that the p53BS possessed p53-dependent transcriptional activity. Colony-formation assays indicated that overexpression of cyclin K suppressed growth of T98G, U373MG and SW480 cells. The results suggested that cyclin K may play a role in regulating the cell cycle or apoptosis after being targeted for transcription by p53.[1]References
- Cyclin K as a direct transcriptional target of the p53 tumor suppressor. Mori, T., Anazawa, Y., Matsui, K., Fukuda, S., Nakamura, Y., Arakawa, H. Neoplasia (2002) [Pubmed]
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