miRNA-103a-3p Promotes Human Gastric Cancer Cell Proliferation by Targeting and Suppressing ATF7 in vitro
Xiaoyi Hu1,2, Jiyu Miao3, Min Zhang4, Xiaofei Wang3, Zhenzhen Wang3, Jia Han3, Dongdong Tong3, and
Chen Huang1,3,*
1Key Laboratory of Shaanxi Province for Craniofacial Precision Medicine Research, College of Stomatology, Xi'an Jiaotong University,
Xi'an, Shaanxi, China, 2Department of Oral Maxillofacial Surgery, Stomatological Hospital, College of Stomatology, Xi'an
Jiaotong University, Xi'an, Shaanxi, China, 3Key Laboratory of Environment and Genes Related to Diseases, College of Medicine,
Xi'an Jiaotong University, Xi'an, Shaanxi, China, 4College of Life Science, Yanan University, Yan’an, Shaanxi, China.
*Correspondence: hchen@mail.xjtu.edu.cn
Received May 15, 2017; Revised February 28, 2018; Accepted March 15, 2018.; Published online May 10, 2018.
© Korean Society for Molecular and Cellular Biology. All rights reserved.

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ABSTRACT
Studies have revealed that miR-103a-3p contributes to tumor growth in several human cancers, and high miR-103a-3p expression is associated with poor prognosis in advanced gastric cancer (GC) patients. Moreover, bioinformatics analysis has shown that miR-103a-3p is upregulated in The Cancer Genome Atlas (TCGA) stomach cancer cohort. These results suggest that miR-103a-3p may function as an oncogene in GC. The present study aimed to investigate the role of miR- 103a-3p in human GC. miR-103a-3p expression levels were increased in 33 clinical GC specimens compared with adjacent nontumor stomach tissues. Gain- and loss-of-function studies were performed to identify the correlation between miR-103a-3p and tumorigenesis in human GC. Inhibiting miR-103a-3p suppressed GC cell proliferation and blocked the S-G2/M transition in MKN-45/SGC-7901 cells, whereas miR-103a-3p overexpression improved GC cell proliferation and promoted the S-G2/M transition in vitro. Bioinformatics and dual-luciferase reporter assays confirmed that ATF7 is a direct target of miR-103a-3p. Analysis of the TCGA stomach cancer cohort further revealed that miR-103a-3p expression was inversely correlated with ATF7 expression. Notably, silencing ATF7 showed similar cellular and molecular effects as miR- 103a-3p overexpression, namely, increased GC cell proliferation, improved CDK2 expression and decreased P27 expression. ATF7 overexpression eliminated the effects of miR-103a-3p expression. These findings indicate that miR-103a-3p promotes the proliferation of GC cell by targeting and suppressing ATF7 in vitro.
Keywords: ATF7, gastric cancer, miRNA-103a-3p, proliferation


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30 April 2018 Volume 41,
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