期刊
BRITISH JOURNAL OF CANCER
卷 91, 期 10, 页码 1808-1812出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/sj.bjc.6602214
关键词
AKT; PTEN; endometrial cancer; apoptosis; experimental therapeutics
类别
资金
- NICHD NIH HHS [2K12HD00849, K12 HD000849] Funding Source: Medline
The PTEN (phosphatase and tensin homolog deleted on chromosome 10) tumour suppressor is mutated in 40-50% of human endometrial cancers. PTEN exerts its effects in part via inhibition of the antiapoptotic protein AKT. We demonstrate that two endometrial cancer cell lines that harbour PTEN mutations, Ishikawa and RL95-2, have high levels of phosphorylated AKT and high AKT kinase activity. Two additional endometrial cancer cell lines that express wild-type PTEN, HecIA and KLE, have little phosphorylated AKT and minimal demonstrable AKT kinase activity. We tested a potential inhibitor of the AKT pathway, API-59CJ-OMe, in these four cell lines. We found that API-59CJ-OMe inhibits AKT kinase activity and induces apoptosis in the Ishikawa and RL95-2 cell lines with high AKT activity, but has little effect on HecIA and KLE cells without AKT activity. API-59CJ-OMe may therefore have therapeutic potential for those endometrial cancers that harbour PTEN mutations and AKT activation.
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