Open AccessDownregulation of ROS1 enhances the therapeutic efficacy of arsenic trioxide in acute myeloid leukemia cell lines
Author(s) -
Jun Li
Publication year - 2018
Publication title -
oncology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.766
H-Index - 54
eISSN - 1792-1082
pISSN - 1792-1074
DOI - 10.3892/ol.2018.8458
Subject(s) - arsenic trioxide , myeloid leukemia , cancer research , oncogene , cell growth , downregulation and upregulation , wnt signaling pathway , gene knockdown , cell cycle , cell , biology , chemistry , apoptosis , signal transduction , microbiology and biotechnology , biochemistry , gene
The present study investigated the function of ROS proto-oncogene 1 receptor tyrosine kinase (ROS1) in regulating the migration and proliferation of acute myeloid leukemia (AML) cells through Wnt/β-catenin signaling, and in arsenic trioxide (ATO) treatment. The migration and proliferation of multiple ROS1-silenced leukemic cell lines was assessed, and the expression levels of proteins associated with Wnt/β-catenin signaling were determined using western blot analysis. Compared with the AML control cells, ROS1-knockdown cells exhibited increased migration and proliferation, and the significant downregulation of β-catenin expression. Additionally, ROS1 knockdown sensitized AML cells to the effects of chemotherapeutic ATO. The results of the present study demonstrated that, in leukemic cell lines, ROS1 counteracted the effects of ATO on migration and proliferation, suggesting that ROS1 may be a potential therapeutic target in patients with AML undergoing ATO treatment. The results of the present study provided novel insight into the function of ATO and ROS1 in regulating AML progression.