@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}
}