期刊
ANTICANCER RESEARCH
卷 37, 期 2, 页码 515-519出版社
INT INST ANTICANCER RESEARCH
DOI: 10.21873/anticanres.11343
关键词
Itraconazole; hedgehog; AKT/mTOR; autophagy; endometrial cancer
类别
资金
- Japan Society for the Promotion of Science KAKENHI [JP16K11166]
- Grants-in-Aid for Scientific Research [16K11166] Funding Source: KAKEN
Background: Itraconazole is a common antifungal agent that has demonstrated anticancer activity in preclinical and clinical studies. This study investigated whether itraconazole exerts this effect in endometrial cancer (EC) cells. Materials and Methods: Cell viability was evaluated with the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, and gene and protein expression were assessed by microarray analysis and immunoblotting, respectively, in five EC cell lines. Results: Itraconazole-suppressed proliferation of AN3-CA, HEC-1A and Ishikawa cells (p < 0.05) but not of HEC-50B or SNG-II cells. Itraconazole did not suppress GLI1 or GLI2 transcription but did inhibit the expression of mammalian target of rapamycin (mTOR) signaling components in AN3-CA and HEC-1A cells, while inducing that of microtubule-associated protein 1A/1B-light chain 3-II, a marker of autophagy. ATP-binding cassette transporter A1 gene was down-regulated in Ishikawa, HEC-50B and SNG-II cells. Conclusion: Itraconazole treatment suppresses the growth of EC cells by inhibiting AKT/mTOR signalling.
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