miR-9-5p Suppresses Malignant Biological Behaviors of Human Gastric Cancer Cells by Negative Regulation of TNFAIP8L3

被引:22
|
作者
Fan, Yanyun [1 ]
Shi, Ying [2 ,3 ]
Lin, Zhenhe [1 ]
Huang, Xiaoxiao [1 ]
Li, Jinying [2 ,3 ]
Huang, Wei [2 ,3 ]
Shen, Dongyan [5 ]
Zhuang, Guohong [4 ]
Liu, Wenming [1 ]
机构
[1] Xiamen Univ, Zhongshan Hosp, Dept Gastroenterol, Xiamen 361004, Fujian, Peoples R China
[2] Jinan Univ, Affiliated Hosp 1, Dept Gastroenterol, Guangzhou 510632, Guangdong, Peoples R China
[3] Jinan Univ, Clin Med Coll 1, Guangzhou 510632, Guangdong, Peoples R China
[4] Xiamen Univ, Med Coll, Organ Transplantat Inst, Xiamen 361005, Fujian, Peoples R China
[5] Xiamen Univ, Affiliated Hosp 1, Biobank, Xiamen 361003, Fujian, Peoples R China
关键词
miR-9-5p; Gastric cancer; Migration; 3 ' UTR; PROLIFERATION; OVEREXPRESSION; INFLAMMATION; EXPRESSION; INVASION; PROTEIN; FAMILY; TIPE3;
D O I
10.1007/s10620-019-05626-2
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Background MicroRNA is essential for the malignant progression of human gastric cancer (GC), which is a leading cause of cancer deaths. However, the mechanism is still not so clear. Aims In our present research, we investigated the effect of miR-9-5p in GC. Methods We detected miR-9-5p expression in human gastric epithelial cell (GES-1) and GC cells (AGS, BGC-823, MKN-45, and MGC-803), plasma of normal or GC patients, as well as orthotopic xenograft mouse models by real-time PCR. The migration ability was detected by Transwell assays after miR-9-5p mimic or inhibitor transfection in GC cells. Results Our results showed that miR-9-5p expression in GC cells and plasma was significantly decreased. miR-9-5p inhibited migration of GC cells by regulating TNFAIP8L3 directly. Low expression of miR-9-5p in GC patients hardly suppressed the migration mediated by TNFAIP8L3. Conclusions miR-9-5p, as a potential tumor suppressor gene, is closely related to the malignant progression of GC. Exploring the regulation between miR-9-5p and TNFAIP8L3 may provide a novel strategy for GC treatment.
引用
收藏
页码:2823 / 2829
页数:7
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