Polo-like kinase 1 (PLK1) is a ubiquitous serine/threonine protein kinase. It is reported to be involved in the occurrence and progression of various human cancers. In the present study, we explored the role and molecular mechanism of PLK1 in the proliferation of osteosarcoma (OS) cells. We found that PLK1 expression was higher in MG63/Dox cells than in MG63 cells, while inhibiting or interfering with the level of PLK1 suppressed cell proliferation of MG63/Dox cells. TargetScan analysis predicted that miR-4779 would interact with the 3′-UTR of PLK1 mRNAs and also inhibit cell autophagy of MG63/Dox cells. The data demonstrated that miR-4779 negatively regulates the expression of PLK1, and both miR-4779 and PLK1 regulate cell proliferation and cell apoptosis of MG63/Dox cells, processes that are involved in the drug resistance of OS cells.

中文翻译：

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PLK1 敲低抑制细胞增殖和细胞凋亡，骨肉瘤细胞中 PLK1 受 miR-4779 负调控。


Polo 样激酶 1 (PLK1) 是一种普遍存在的丝氨酸/苏氨酸蛋白激酶。据报道它参与多种人类癌症的发生和进展。在本研究中，我们探讨了PLK1在骨肉瘤（ OS ）细胞增殖中的作用和分子机制。我们发现PLK1在MG63/Dox细胞中的表达高于MG63细胞，而抑制或干扰PLK1的水平则抑制了MG63/Dox细胞的细胞增殖。 TargetScan 分析预测 miR-4779 会与 PLK1 mRNA 的 3'-UTR 相互作用，并抑制 MG63/Dox 细胞的细胞自噬。数据表明，miR-4779负向调节PLK1的表达，并且miR-4779和PLK1均调节MG63/Dox细胞的细胞增殖和细胞凋亡，这些过程涉及OS细胞的耐药性。