MicroRNA-532-3p Suppresses Malignant Behaviors of Tongue Squamous Cell Carcinoma via Regulating CCR7

被引:28
作者
Feng, Cuijuan [1 ]
So, Hyon Il [2 ]
Yin, Shoucheng [3 ]
Su, Xingzhou [3 ]
Xu, Qiang [3 ]
Wang, Simin [3 ]
Duan, Weiyi [3 ]
Zhang, Enjiao [3 ]
Sun, Changfu [3 ]
Xu, Zhongfei [3 ]
机构
[1] China Med Univ, Sch Stomatol, Dept Orthodont, Shenyang, Liaoning, Peoples R China
[2] Kim IL Sung Univ, Pyongyang Med Coll, Dept Oral & Maxillofacial Surg, Pyongyang, North Korea
[3] China Med Univ, Sch Stomatol, Dept Oral & Maxillofacial Surg, Shenyang, Liaoning, Peoples R China
关键词
microRNA-532-3p; CCR7; tongue squamous cell carcinoma; proliferation; migration; invasion; apoptosis; MESENCHYMAL TRANSITION; SIGNALING PATHWAY; CANCER CELLS; METASTASIS; MIGRATION; PROGNOSIS; PROMOTES; PTEN; PROLIFERATION; ACTIVATION;
D O I
10.3389/fphar.2019.00940
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
To provide better therapeutic avenues for treating tongue squamous cell carcinoma (TSCC), a series of experiments about the effects of microRNA (miR)-532-3p on TSCC malignant behaviors were carried out. The result showed that miR-532-3p was down-regulated and C-C chemokine receptor 7 (CCR7) was up-regulated in the tumor tissues compared with those in the paired paratumor tissues. Further, expression of miR-532-3p was detected in four TSCC cell lines, TSCCA, TCA8113, CAL-27, and SCC-25. The miR-532-3p mimics and inhibitor were transfected into the CAL-27 and TCA8113 cell lines which were the relatively lowest and highest miR-532-3p expressions, respectively. It was found that the overexpression of miR-532-3p suppressed TSCC cell proliferation, migration, invasion, and promoted apoptosis in vitro, whilst the knockdown of miR-532-3p reversed these behaviors. The bioinformatics predicted that CCR7 was a downstream gene of miR-532-3p, which was confirmed via luciferase assay. Following, the decline of CCR7 in the miR-532-3p mimics group and the rise of CCR7 in the miR-532-3p inhibitor group were also verified. In addition, enhanced cell proliferation, migration and invasion induced by CCR7 were partly restrained by miR-532-3p in TSCC cell. Meanwhile, miR-532-3p attenuated tumourigenesis in vivo due to the reduction of tumor volume and Ki-67 positive rate and the increase of apoptotic cells. Taken together, these findings reveal a pivotal role for the miR-532-3p/CCR7 axis in regulating TSCC, and this novel axis could be suitable for therapeutic intervention in TSCC disease.
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页数:11
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