@Article{096504019X15528367532612, AUTHOR = {Zhiguo Wang, Zehui Fang, Runzhang Lu, Hongli Zhao, Tiejun Gong, Dong Liu, Luojia Hong, Jun Ma, Mei Zhang}, TITLE = {MicroRNA-204 Potentiates the Sensitivity of Acute Myeloid Leukemia Cells to Arsenic Trioxide}, JOURNAL = {Oncology Research}, VOLUME = {27}, YEAR = {2019}, NUMBER = {9}, PAGES = {1035--1042}, URL = {http://www.techscience.com/or/v27n9/48632}, ISSN = {1555-3906}, ABSTRACT = {Although arsenic trioxide (ATO) is a well-known antileukemic drug used for acute promyelocytic leukemia treatment, the development of ATO resistance is still a big challenge. We previously reported that microRNA- 204 (miR-204) was involved in the regulation of acute myeloid leukemia (AML) cell apoptosis, but its role in chemoresistance is poorly understood. In the present study, we showed that miR-204 was significantly increased in AML cells after ATO treatment. Interestingly, the increased miR-204 level that was negatively correlated with ATO induced the decrease in cell viability and baculoviral inhibition of apoptosis protein repeatcontaining 6 (BIRC6) expression. Overexpression of miR-204 potentiated ATO-induced AML cell growth inhibition and apoptosis. Furthermore, miR-204 directly targets to the 3 -UTR of BIRC6. Upregulation of miR-204 decreased BIRC6 luciferase activity and expression, which subsequently enhanced the expression of p53. Restoration of BIRC6 markedly reversed the effect of miR-204 on the regulation of AML cell sensitivity to ATO. Taken together, our study demonstrates that miR-204 decreases ATO chemoresistance in AML cells at least partially via promoting BIRC6/p53-mediated apoptosis. miR-204 represents a novel target of ATO, and upregulation of miR-204 may be a useful strategy to improve the efficacy of ATO in AML treatment.}, DOI = {10.3727/096504019X15528367532612} }