MiR-1299 functions as a tumor suppressor to inhibit the proliferation and metastasis of gastric cancer by targeting ARF6

被引:5
|
作者
Qiu, Yang [1 ]
Yuan, Yonggang [2 ]
Luo, Ping [3 ]
机构
[1] Jiangxi Canc Hosp, Dept Radiotherapy, Nanchang 330029, Jiangxi, Peoples R China
[2] Peoples Hosp Lujiang Cty, Dept Oncol, Hefei 231500, Anhui, Peoples R China
[3] Nanchang Third Hosp, Dept Breast Surg, Nanchang 330002, Jiangxi, Peoples R China
关键词
MiR-1299; ARF6; Gastric cancer; Proliferation; Apoptosis; CELL-PROLIFERATION; HEPATOCELLULAR-CARCINOMA; MICRORNAS;
D O I
10.1007/s13258-021-01124-w
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Background MiRNAs belong to non-coding RNAs that are involved in cancer development. Acting as a mediator, they could regulate the expression level of numerous gens. However, the expression and function of miR-1299 in gastric cancer (GC) are not clear. Objective To explore the role of miR-1299 in the process of GC. Methods We detected the levels of miR-1299 in clinical samples of GC and investigated the role of miR-1299 in the regulation of the GC cells proliferation, apoptosis and metastasis. Luciferase reporter assay was employed to verify the target of miR-1299. Additionally, the proliferation, apoptosis and metastasis of AGS and SGC7901 cells were analyzed after the overexpression of miR-1299. Results Our study showed the expression of miR-1299 was decreased in GC tissues and cell lines. It indicated that the cell proliferation, migration and invasion was inhibited, while the cell apoptosis was promoted by the over-expressed miR-1299. Also, we found that miR-1299 could directly target the 3 '-untranslated region (3 ' UTR) of ARF6 genes. In addition, rescue assay demonstrated that miR-1299 overexpression promoted the cell apoptosis and inhibited cell growth, which could be attenuated by the overexpression of ARF6. Conclusions These findings indicate that miR-1299 regulates cell progression in GC by targeting ARF6 genes, and suggest that miR-1299 may be a tumor suppressor in the GC progression.
引用
收藏
页码:237 / 245
页数:9
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