TY - JOUR T1 - Itraconazole Inhibits AKT/mTOR Signaling and Proliferation in Endometrial Cancer Cells JF - Anticancer Research JO - Anticancer Res SP - 515 LP - 519 VL - 37 IS - 2 AU - HIROSHI TSUBAMOTO AU - KAYO INOUE AU - KAZUKO SAKATA AU - TOMOKO UEDA AU - RYU TAKEYAMA AU - HIROAKI SHIBAHARA AU - TAKASHI SONODA Y1 - 2017/02/01 UR - http://ar.iiarjournals.org/content/37/2/515.abstract N2 - 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. ER -