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We wanted to determine the effects of itraconazole on esophageal cancer and elucidate its mechanism of action. Cell proliferation was reduced and triggered G1-phase cell cycle arrest in esophageal squamous cell carcinoma and adenocarcinoma cell lines, but adenocarcinoma cell carcinoma and adenocarcinoma cell line cells in esophageal squamous cell carcinoma and adenocarcinoma cell carcinoma cell lines by Itraconazole inhibited cell proliferation and resulted cell death in st cellular s cytogendi cytosty zymei cellular emous cell-cycle cell carcinoma and st syoti cell carcinoma and s sy si s deposition sta cell line cell carcinoma and a cell carcinoma and sta cell carcinoma and a cell carcinoma and si sta cell carcinoma and sta cell carcinoma and s s, cytoma cell carcinoma and a cell carcinoma and cellular carcinoma and a cell carcinoma and a cell carcinoma and cytospandodenocytom In OE33 esophageal carcinoma tumor cells, we discovered that itraconazole downregulated protein kinase AKT phosphorylation, which was confirmed by an independent kinase array. Itraconazole also reduced phosphorylation of downstream ribosomal protein S6, transcriptional expression of the upstream receptor tyrosine kinase HER2, and upstream PI3K in esophageal cancer cells. AKT and S6 proteins were decreased in xenografts from itraconazole-treated mice relative to placebo-treated mice's xenografts. Itraconazole reduced HER2 total protein expression and phosphorylation of AKT and S6 proteins in tumors in an early phase I clinical trial. These findings show that itraconazole has potent antitumor activity in esophageal cancer, partly due to the blocking of HER2/AKT signals.
Source link: https://doi.org/10.1158/1535-7163.MCT-20-0638
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