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논문 기본 정보

자료유형
학술저널
저자정보
Xiaoyi Hu (Xi'an Jiaotong University) Jiyu Miao (Xi'an Jiaotong University) Min Zhang (Yanan University) Xiaofei Wang (Xi'an Jiaotong University) Zhenzhen Wang (Xi'an Jiaotong University) Jia Han (Xi'an Jiaotong University) Dongdong Tong (Xi'an Jiaotong University) Chen Huang (Xi'an Jiaotong University)
저널정보
한국분자세포생물학회 Molecules and Cells Molecules and Cells 제41권 제5호
발행연도
2018.3
수록면
390 - 400 (11page)
DOI
10.14348/molcells.2018.2078

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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. Bioin-formatics 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.

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