@Article{096504016X14732772150541,
AUTHOR = {Xiangrui Meng, Xiaoqi Chen, Peng Lu, Wang Ma, Dongli Yue, Lijie Song, Qingxia Fan},
TITLE = {miR-202 Promotes Cell Apoptosis in Esophageal Squamous  Cell Carcinoma by Targeting HSF2},
JOURNAL = {Oncology Research},
VOLUME = {25},
YEAR = {2017},
NUMBER = {2},
PAGES = {215--223},
URL = {http://www.techscience.com/or/v25n2/56800},
ISSN = {1555-3906},
ABSTRACT = {Esophageal squamous cell carcinoma (ESCC) is one of the most common malignant cancers with high mortality 
around the world. However, the regulatory mechanism of ESCC carcinogenesis is not completely known. Here 
we demonstrate the novel role of miR-202 in regulating ESCC cell apoptosis. The analysis of data obtained 
from the GEO database showed that the expression of miR-202 is aberrantly decreased in tumor tissue from 
ESCC patients and cultured ESCC cell lines. After transfection with miR-202 mimic or inhibitor, the apoptotic capacity of ESCC cells was significantly increased by miR-202 overexpression but reduced by miR-202 
repression. We then identified HSF2 as a direct target of miR-202 with the binding site on the 3¢-UTR of HSF2 
mRNA in ESCC cells. The apoptosis of ESCC cells induced by the miR-202 mimic could be repressed by 
HSF2 overexpression. Further studies indicated that HSF2 overexpression strongly upregulated the expression 
of Hsp70 at both the mRNA and protein levels. In addition, HSF2/Hsp70 suppressed ESCC cell apoptosis by 
preventing caspase 3 activation. In conclusion, miR-202 is a potential tumor suppressor in human ESCC and 
acts by regulating the apoptosis of ESCC cells by targeting HSF2, in which caspase 3 activation is involved. 
This might provide a novel therapeutic target for human ESCC.},
DOI = {10.3727/096504016X14732772150541}
}