Inhibition of AKT survival pathway by a small molecule inhibitor in human endometrial cancer cells

X. Jin, D. R. Gossett, S. Wang, D. Yang, Y. Cao, J. Chen, R. Guo, R. K. Reynolds, J. Lin*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

66 Scopus citations


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, Hecl A 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 Heel A 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.

Original languageEnglish (US)
Pages (from-to)1808-1812
Number of pages5
JournalBritish Journal of Cancer
Issue number10
StatePublished - Nov 15 2004


  • AKT
  • Apoptosis
  • Endometrial cancer
  • Experimental therapeutics
  • PTEN

ASJC Scopus subject areas

  • Oncology
  • Cancer Research


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