circPTK2调控miR-619-5p对食道癌细胞侵袭迁移的影响

doi:10.3969/j.issn.1006-6233.2022.11.04

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Abstract Objective: To investigate the effect of circPTK2 on the invasion and migration of esophageal cancer (EC) cells by regulating miR-619-5p.Methods: QRT-PCR was performed to measure the expressions of circPTK2 and miR-619-5p in EC tissues and cell lines (OE19, KYSE-450, KYSE-520, TE-13). TE-13 cells were randomly separated into control group, si-NC, si-circPTK2 group, miR-NC group, miR-619-5p group, si-circPTK2+anti-NC group and si-circPTK2+anti-miR-619- 5p group. Cell viability analysis was performed with Cell Counting Box-8 (CCK-8); the cell invasion and migration ability were measured by Transwell assay; the expression of epithelial-mesenchymal transition (EMT)-related proteins (E-cadherin, N-cadherin, Vimentin) was measureed by western blot. The interaction between circPTK2 and miR-619-5p was verified by dual-luciferase reporter gene assay and RNA pull-down experiment. The role of circPTK2 in vivo was investigated using xenograft experiments. Results: The expression of circPTK2 was up-regulated in EC tissues and cells, and the expression of miR-619-5p was down-regulated (P<0.05). Downregulation of circPTK2 expression or overexpression of miR-619-5p inhibited cell growth, invasion, migration and EMT (P<0.05). MiR-619-5p was a target of circPTK2. Inhibition of miR-619-5p reversed the effects of circPTK2 downregulation on EC cell proliferation, invasion, migration and EMT (P<0.05). In addition, inhibition of miR-619-5p expression could partially restore the effect of downregulation of circPTK2 on tumor growth (P<0.05). Conclusion: CircPTK2 promotes the growth, invasion and migration of EC cells through sponge adsorption of miR-619-5p, circPTK2 may become a potential therapeutic target for EC metastasis and is a promising biomarker for predicting EC cell metastasis.

Key words： circPTK2 miR-619-5p Esophageal cancer Invasion Migration

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http://www.hbyxzzs.cn/EN/10.3969/j.issn.1006-6233.2022.11.04 OR http://www.hbyxzzs.cn/EN/Y2022/V28/I11/1778

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