Objective

PTK2 has been reported to be involved in tumor progression, but its regulating mechanisms in cervical cancer (CC) remain to be elusive. MiRNA-520d-5p was demonstrated to regulate the expression of many genes and inhibit the development of human tumors. However, the functional mechanisms of miRNA-520d-5p in the regulation of cervical cancer are not fully understood.

Methods

RT-qPCR was employed to detect the expression levels of miR-520d-5p and PTK2. Western blot was performed to detect the expression levels of proteins. Dual-luciferase reporter assay was utilized to investigate the associations between miR-520d-5p and PTK2. CCK-8 assay was carried out to measure cell proliferation. In addition, transwell assay and scratch assay were used for cell invasion and migration analysis. Flow cytometry was used to detect cell apoptosis of cervical cancer.

Results

The expression levels of PTK2 were elevated in CC tissues and cells lines. It was found that PTK2 was a target gene of miR-520d-5p. The expression of miR-520d-5p was down-regulated in CC tissues, which was negatively correlated with the expression of PTK2. MiR-520d-5p inhibited the proliferation, migration, and invasion of CC cells. In addition, overexpression of miR-520d-5p resulted in apoptosis of CC cells. Finally, we demonstrated that miR-520d-5p inhibited the activation of PI3K/AKT signaling.

Conclusion

MiR-520d-5p suppressed the proliferation, invasion, and migration of CC cells via targeting PTK2.

中文翻译：

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通过靶向PTK2，MiR-520d-5p在宫颈癌中起着抑癌基因的作用。

目的

据报道，PTK2参与了肿瘤的进展，但其在宫颈癌（CC）中的调控机制仍然不清楚。MiRNA-520d-5p被证明可调节许多基因的表达并抑制人类肿瘤的发展。但是，miRNA-520d-5p在宫颈癌调控中的功能机制尚不完全清楚。

方法

用RT-qPCR检测miR-520d-5p和PTK2的表达水平。进行蛋白质印迹以检测蛋白质的表达水平。利用双重荧光素酶报告基因测定来研究miR-520d-5p与PTK2之间的关联。进行CCK-8测定以测量细胞增殖。此外，transwell分析和划痕分析用于细胞侵袭和迁移分析。流式细胞仪用于检测宫颈癌的细胞凋亡。

结果

PTK2在CC组织和细胞系中的表达水平升高。发现PTK2是miR-520d-5p的靶基因。CC组织中miR-520d-5p的表达下调，与PTK2的表达呈负相关。MiR-520d-5p抑制CC细胞的增殖，迁移和侵袭。此外，miR-520d-5p的过表达导致CC细胞凋亡。最后，我们证明了miR-520d-5p抑制了PI3K / AKT信号的激活。

结论

MiR-520d-5p通过靶向PTK2抑制CC细胞的增殖，侵袭和迁移。