Objective. The abnormal expression of epithelial cell transforming sequence 2 (ECT2) is often considered the driving factor for the growth and invasion of tumors. This study was performed to investigate the regulatory effect of miR-30a-5p and ECT2 on lung adenocarcinoma (LUAD), which provides a basis for the effective clinical treatment of LUAD. Methods. The mature miRNAs, expression data of mRNAs, and clinical data of LUAD were downloaded from The Cancer Genome Atlas (TCGA). The expression levels of ECT2 mRNA and miR-30a-5p in cancer cell lines were detected by qRT-PCR. Western blot was performed to test the expression of ECT2 protein. The targeting relationship between miR-30a-5p and ECT2 was verified by dual-luciferase assay. The CCK-8 method and Transwell assay were conducted to test the viability, migratory, and invasive abilities of cells. Results. ECT2 expression was upregulated in LUAD and was significantly correlated with the LUAD clinical stage and pathologic T stage, and the expression of its upstream regulatory gene miR-30a-5p was downregulated. miR-30a-5p targeted ECT2 in LUAD. Downregulation of ECT2 could inhibit the viability, migration, and invasion of LUAD cells, which could be reversed by simultaneously suppressing the expression of miR-30a-5p. Conclusion. Our results suggested that miR-30a-5p repressed the malignant progression of LUAD via downregulating ECT2. miR-30a-5p and ECT2 may be effective targets for LUAD patients.

中文翻译：

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miR-30a-5p 通过靶向 ECT2 调节肺腺癌细胞的活力、迁移和侵袭

客观的。上皮细胞转化序列2（ECT2）的异常表达通常被认为是肿瘤生长和侵袭的驱动因素。本研究旨在探讨miR-30a-5p和ECT2对肺腺癌（LUAD）的调控作用，为临床有效治疗LUAD提供依据。方法。LUAD的成熟miRNA、mRNA表达数据和临床数据均从癌症基因组图谱（TCGA）下载。采用qRT-PCR检测癌细胞系中ECT2 mRNA和miR-30a-5p的表达水平。Western blot检测ECT2蛋白的表达。通过双荧光素酶测定验证了 miR-30a-5p 和 ECT2 之间的靶向关系。采用CCK-8法和Transwell实验检测细胞的活力、迁移和侵袭能力。结果。ECT2在LUAD中表达上调，且与LUAD临床分期和病理T分期显着相关，其上游调控基因miR-30a-5p表达下调。miR-30a-5p 靶向 LUAD 中的 ECT2。ECT2 的下调可以抑制 LUAD 细胞的活力、迁移和侵袭，这可以通过同时抑制 miR-30a-5p 的表达来逆转。结论。我们的结果表明，miR-30a-5p 通过下调 ECT2 抑制 LUAD 的恶性进展。miR-30a-5p 和 ECT2 可能是 LUAD 患者的有效靶点。