Abstract
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.
Highlights
Lung cancer is a leading cause of cancer-related deaths worldwide, and lung adenocarcinoma (LUAD) takes up about 50% of all lung cancer cases, with an increasing trend year by year [1]
In order to explore the expression of epithelial cell transforming sequence 2 (ECT2) in LUAD, bioinformatics analysis was first performed to obtain 3611 differentially expressed mRNAs (Figure 1(a)), and ECT2 was highly expressed in LUAD tissue (Figure 1(b))
Hirata et al [13] revealed that the downregulation of ECT2 expression could effectively suppress the growth of lung cancer cells, and they found that ECT2 plays a regulatory role in cell cycle progression and cell division
Summary
Lung cancer is a leading cause of cancer-related deaths worldwide, and lung adenocarcinoma (LUAD) takes up about 50% of all lung cancer cases, with an increasing trend year by year [1]. LUAD is a type of non-small-cell lung cancer (NSCLC), most of which originate from the bronchial mucosal epithelium, and a few originate from the large bronchial mucous glands. Despite the recent advances in diagnosis and treatment strategies of LUAD, treatment failures are still common in patients with advanced LUAD [3]. To solve this problem, many researchers have carried out indepth research and investigation. Studies on genetics and epigenetics of LUAD reveal that epithelial cell transforming sequence 2 (ECT2) is differentially expressed in both adenocarcinoma in situ (AIS) and early invasive adenocarcinoma [4], suggesting that ECT2 may be a new entry point for LUAD treatment
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