Lung adenocarcinoma (LUAD) is the most prevalent histological subclass of non-small cell lung cancer. Long non-coding RNAs (lncRNAs) have been recognized as the crucial regulatory factors in tumor development and progression. Nevertheless, limited research has been carried on the function of PRKCZ-AS1 in LUAD. In this study, the expression of PRKCZ-AS1 in LUAD tissues and cell lines was notably upregulated. Moreover, knockdown of PRKCZ-AS1 inhibited the proliferation and migration, but promoted apoptosis in LUAD cells. Furthermore, miR-766-5p could bind with PRKCZ-AS1. Besides, the expression miR-766-5p was negatively regulated by PRKCZ-AS1 expression in LUAD cells. Furtherly, PRKCZ-AS1 expression positively regulated the expression of MAPK1. Similarly, the expression of MAPK1 was negatively regulated by miR-766-5p expression. Moreover, the binding ability between miR-766-5p and MAPK1 was confirmed. Furthermore, knockdown of MAPK1 partly rescued the miR-766-5p inhibition-mediated promoting effect on proliferation and migration in LUAD cells transfected with PRKCZ-AS1#1. Overall, above results suggested that PRKCZ-AS1 promotes the occurrence of LUAD by sponging miR-766-5p to upregulate MAPK1 expression, which may provide new insights into LUAD treatment.

中文翻译：

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PRKCZ-AS1通过海绵miR-766-5p调节MAPK1促进肺腺癌的发生。

肺腺癌 (LUAD) 是非小细胞肺癌最常见的组织学亚类。长链非编码 RNA (lncRNA) 已被公认为是肿瘤发生发展的关键调控因子。然而，对 PRKCZ-AS1 在 LUAD 中的功能的研究有限。在本研究中，PRKCZ-AS1 在 LUAD 组织和细胞系中的表达显着上调。此外，PRKCZ-AS1 的敲低抑制了 LUAD 细胞的增殖和迁移，但促进了细胞凋亡。此外，miR-766-5p 可以与 PRKCZ-AS1 结合。此外，在LUAD细胞中，miR-766-5p的表达受到PRKCZ-AS1表达的负调控。此外，PRKCZ-AS1 表达正调控 MAPK1 的表达。同样，MAPK1 的表达受到 miR-766-5p 表达的负调控。而且，证实了 miR-766-5p 与 MAPK1 之间的结合能力。此外，MAPK1 的敲低部分挽救了 miR-766-5p 抑制介导的对 PRKCZ-AS1#1 转染的 LUAD 细胞增殖和迁移的促进作用。总体而言，上述结果表明 PRKCZ-AS1 通过海绵 miR-766-5p 上调 MAPK1 表达来促进 LUAD 的发生，这可能为 LUAD 治疗提供新的见解。