MicroRNA-488 inhibits proliferation, invasion and EMT in osteosarcoma cell lines by targeting aquaporin 3

MicroRNA-488 通过靶向水通道蛋白 3 抑制骨肉瘤细胞系的增殖、侵袭和 EMT

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作者:Jing Qiu, Yongzhi Zhang, Hu Chen, Zhi Guo

Abstract

It has been reported that aquaporin 3 (AQP3) expression is associated with the progression of numerous types of cancer and microRNA (miRNA/miR) processing. However, the effects and precise mechanisms of AQP3 in osteosarcoma (OS) have not been fully elucidated. The present study aimed to investigate the interaction between AQP3 and miR‑488 in OS. The reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) assay was performed to detect the levels of AQP3 and miR‑488 in OS tissues and cell lines, respectively. Cell proliferation, invasion and epithelial-mesenchymal transition (EMT) were detected to analyze the biological functions of miR‑488 and AQP3 in OS cells. Furthermore, mRNA and protein levels of AQP3 was measured by RT‑qPCR and western blot analysis. Furthermore, AQP3 was validated as an miR‑488 target using luciferase assays in OS cells. The present study revealed that the miR‑488 level was significantly downregulated in OS tissues and cell lines, and that the expression of AQP3 was markedly increased. Notable, the low miR‑488 expression level was associated with upregulated AQP3 expression in OS tissues. Furthermore, introduction of miR‑488 markedly suppressed the proliferation, invasion and EMT of OS cells. However, miR‑488-knockdown increased the proliferation, invasion and EMT of OS cells. The present study demonstrated that miR‑488 could directly target AQP3 using bioinformatics analysis and luciferase reporter assays. In addition, AQP3-silencing had similar effects to miR‑488 overexpression on OS cells. Overexpression of AQP3 in OS cells partially reversed the inhibitory effects of miR‑488 mimic. miR‑488 inhibited the proliferation, invasion and EMT of OS cells by directly downregulating AQP3 expression, and miR‑488 targeting AQP3 was responsible for inhibition of the proliferation, invasion and EMT of OS cells.

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