Journal
ONCOGENE
Volume 35, Issue 28, Pages 3669-3680Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/onc.2015.432
Keywords
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Funding
- National Cheng Kung University project of the Program for Promoting Academic Excellence and Developing World Class Research Centers
- Ministry of Science and Technology, Taiwan [MOST 103-2320-B-006-035-MY3, MOST 103-2321-B-006-023-MY3]
- National Research Program for Biopharmaceuticals of National Science Council, Taiwan
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Ubiquitin is a critical modifier regulating the degradation and function of its target proteins during posttranslational modification. Here we found that ubiquitin-specific peptidase 24 (USP24) is highly expressed in cell lines with enhanced malignancy and in late-stage lung cancer clinical samples. Studying single-nucleotide polymorphisms (SNPs) of USP24 using genomic DNA of lung cancer patients revealed an increase in SNP 7656C/T. When using RNA specimens instead of the genomic DNA of lung cancer patients, we found significant increases in the ratios of variants 930C/T and 7656T/C, suggesting that variants at these two sites are not only caused by the SNP of DNA but also by the RNA editing. USP24-930T and USP24-7656C increase USP24 expression levels by increasing RNA stability. Knocking down USP24 increased Suv39h1 level through a decrease in mouse double-minute 2 homolog levels, thus enhancing lysine-9 methylation of histone H3, and resulting in the prevention of lung cancer malignancy. In conclusion, as USP24 variant analysis revealed a higher ratio of variants in blood specimens of lung cancer patients than that in normal individuals, USP24-930T and USP24-7656C might be useful as diagnostic markers for cancer detection.
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