LncRNA SNHG3 promoted cell proliferation, migration, and metastasis of esophageal squamous cell carcinoma via regulating miR-151a-3p/PFN2 axis

被引:1
作者
Ren, Tiejun [1 ]
Wang, Dingyi [2 ]
Gu, Jinjin [2 ]
Hou, Xiaozhen [2 ]
机构
[1] Zhengzhou Univ, Luoyang Cent Hosp, Dept Med Oncol, 288 Zhongzhou Middle Rd, Luoyang 471000, Henan, Peoples R China
[2] Xinxiang Med Univ, Dept Med Oncol, Xinxiang 453003, Henan, Peoples R China
来源
OPEN MEDICINE | 2022年 / 17卷 / 01期
关键词
esophageal squamous cell carcinoma; lncRNA SNHG3; miR-151a-3p; PFN2; LUNG-CANCER; PROGRESSION; INVASION;
D O I
10.1515/med-2022-0548
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Esophageal squamous cell carcinoma (ESCC) is an aggressive malignant tumor with a poor prognosis. The dysregulation of long non-coding RNAs (lncRNAs) is closely related to the tumorigenesis and progression of ESCC. However, the effects of lncRNA small nucleolar RNA host gene 3 (lncRNA SNHG3) in ESCC are still unclear. Therefore, a series of experiments methods, such as quantitative real-time polymerase chain reaction, function gain/loss experiments, western blots, and animal xenograft tumor model, were employed to explore the biological function and molecular mechanism of SNHG3 in ESCC. As results, we first reported that SNHG3 was significantly up-regulated in ESCC tissues and cells. SNHG3 knockdown obviously inhibited cell proliferation, migration, invasion, and promoted apoptosis. Mechanism analysis revealed that SNHG3 sponged miR-151a-3p to regulate PFN2. Inhibition of miR-151a-3p and overexpression of PFN2 attenuated the positive effect of SNHG3 knockdown on suppressing tumor progression. Furthermore, the anti-tumor effects of SNHG3 knockdown were also observed in vivo. In summary, our results indicated that SNHG3 knockdown suppressed tumor development via the miR-151a-3p/PFN2 axis, and targeting SNHG3 may provide a new opportunity for ESCC patients.
引用
收藏
页码:1584 / 1598
页数:15
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