Lung adenocarcinoma (LUAD) severely affects human health, and cisplatin (DDP) resistance is the main obstacle in LUAD treatment, the mechanism of which is unknown. Bioinformatics methods were utilized to predict expression and related pathways of AURKB in LUAD tissues, as well as the upstream regulated microRNAs. qRT-PCR assayed expression of AURKB and microRNA-486-5p. RIP and dual-luciferase experiments verified the binding and interaction between the two genes. CCK-8 was used to detect cell proliferation ability and IC₅₀ values. Flow cytometry was utilized to assess the cell cycle. Comet assay and western blot tested DNA damage and γ−H2AX protein expression, respectively. In LUAD, AURKB was upregulated, but microRNA-486-5p was downregulated. The targeted relationship between the two was confirmed by RIP and dual-luciferase experiments. Cell experiments showed that AURKB knock-down inhibited cell proliferation, reduced IC₅₀ values, induced cell cycle arrest, and caused DNA damage. The rescue experiment presented that high expression of microRNA-486-5p could weaken the impact of AURKB overexpression on LUAD cell behavior and DDP resistance. microRNA-486-5p regulated DNA damage to inhibit DDP resistance in LUAD by targeting AURKB, implying that microRNA-486-5p/AURKB axis may be a possible therapeutic target for DDP resistance in LUAD patients.

中文翻译：

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microRNA-486-5p 通过靶向 AURKB 调节肺腺癌的 DNA 损伤抑制和顺铂耐药性

肺腺癌（LUAD）严重影响人类健康，顺铂（DDP）耐药是LUAD治疗的主要障碍，其机制尚不清楚。利用生物信息学方法预测LUAD组织中AURKB的表达及相关通路，以及上游调控的microRNA。 qRT-PCR 测定了 AURKB 和 microRNA-486-5p 的表达。 RIP和双荧光素酶实验验证了两个基因之间的结合和相互作用。 CCK-8检测细胞增殖能力和IC ₅₀值。利用流式细胞术评估细胞周期。彗星试验和蛋白质印迹分别测试了 DNA 损伤和γ -H2AX 蛋白表达。在 LUAD 中，AURKB 上调，但 microRNA-486-5p 下调。 RIP和双荧光素酶实验证实了两者之间的靶向关系。细胞实验表明，AURKB敲低可抑制细胞增殖、降低IC ₅₀值、诱导细胞周期停滞并引起DNA损伤。拯救实验表明，microRNA-486-5p的高表达可以减弱AURKB过表达对LUAD细胞行为和DDP抵抗的影响。 microRNA-486-5p 通过靶向 AURKB 调节 DNA 损伤来抑制 LUAD 中的 DDP 耐药，这意味着 microRNA-486-5p/AURKB 轴可能是 LUAD 患者 DDP 耐药的可能治疗靶点。