Abstract：
Lung adenocarcinoma (LUAD) is a predominant malignancy, and its high mortality prompts us to incessantly probe the relevant targeted treatment. This work intended to study the molecular mechanism of ESPL1 in LUAD. Bioinformatics analysis was performed for pan-cancer and prognosis analysis as well as target gene prediction. Expression of ESPL1 mRNA and let-7c-5p was determined via qRT-PCR, and western blot was employed to detect protein level of ESPL1. Dual-luciferase reporter gene method verified the interaction between ESPL1 and let-7c-5p. Thereafter, CCK-8, wound healing, Transwell, and flow cytometry assays were utilized to investigate proliferation, migration, and apoptosis of LUAD cells. The results revealed that ESPL1 was upregulated in LUAD, which was associated with poor prognosis. Overexpressed ESPL1 promoted LUAD cells to invade, proliferate, and migrate. Furthermore, ESPL1 was a target gene of let-7c-5p. Let-7c-5p was downregulated in LUAD cells, and played a suppressive role in LUAD malignant development, while reversed by ESPL1. Taken together, it was posited that let-7c-5p/ESPL1 may be underlying therapeutic targets of LUAD.
摘要：
肺腺癌（LUAD）是一种主要的恶性肿瘤，其高死亡率促使我们不断探索相关的靶向治疗。本工作旨在研究ESPL1在LUAD中的分子机制。生物信息学分析用于泛癌症和预后分析以及靶基因预测。通过qRT-PCR检测ESPL1mRNA和let-7c-5p的表达,采用蛋白质印迹法检测ESPL1蛋白水平。双荧光素酶报告基因方法验证了ESPL1和let-7c-5p之间的相互作用。此后,CCK-8，伤口愈合，Transwell,和流式细胞术测定用于研究增殖，迁移,以及LUAD细胞的凋亡。结果表明，在LUAD中ESPL1上调，这与不良预后有关。ESPL1过表达促进LUAD细胞侵入，增殖，和迁移。此外，ESPL1是let-7c-5p的靶基因。Let-7c-5p在LUAD细胞中下调,并在LUAD恶性发展中起抑制作用，而由ESPL1逆转。一起来看,认为let-7c-5p/ESPL1可能是LUAD的潜在治疗靶点.
