Abstract
Lung adenocarcinoma (LUAD) is one of the most lethal malignancies, posing a threat to human health. However, the molecular mechanisms underlying LUAD development remain largely unknown. In this study, we found that miR-1-3p was significantly downregulated in human LUAD tissues and cell lines and played an inhibitory role in LUAD cell tumorigenesis, as evidenced by the significantly reduced viability, migration, and invasion of LUAD cells in response to miR-1-3p overexpression. Mechanistically, microRNA (miR)-1-3p physically interacted with the 3′-untranslated region (UTR) of protein regulator of cytokinesis 1 (PRC1) mRNA, leading to downregulation of PRC1. Overexpression of PRC1 reversed the inhibitory effects of miR-1-3p on LUAD cell tumorigenesis, suggesting that the miR-1-3p/PRC1 axis is majorly involved in suppressing LUAD development and progression. Consistently, PRC1 was dramatically induced in LUAD tissues and cell lines as well as associated with a poor prognosis in LUAD patients. Taken together, our study identified the miR-1-3p/PRC1 axis as an important regulatory mechanism contributing to LUAD inhibition and provided valuable clues for the future development of therapeutic strategies against LUAD.
Highlights
Lung adenocarcinoma (LUAD) is the most common subtype of non-small cell lung cancer (NSCLC), accounting for 80–85% of all lung cancers; worldwide, approximately 40% of all lung cancer patients are diagnosed with LUAD [1]
These results demonstrate that miR-1-3p is sufficient to suppress LUAD cell growth in vitro
The results demonstrated that the protein regulator of cytokinesis 1 (PRC1) 3′-untranslated region (UTR) mutation had no significant effect on the luciferase activity in miR-13p-transfected LUAD cells, compared with that in the NCtransfected cells (Figure 5F), suggesting that WT PRC1 3′-UTR is essential for the function of miR-1-3p
Summary
Lung adenocarcinoma (LUAD) is the most common subtype of non-small cell lung cancer (NSCLC), accounting for 80–85% of all lung cancers; worldwide, approximately 40% of all lung cancer patients are diagnosed with LUAD [1]. Compared to other subtypes of NSCLC, LUAD has a higher incidence and a shorter survival time among patients, with a 5-year survival rate as low as 10–15% [2, 3]; LUAD poses a serious threat to human health. A variety of miRNAs have been identified as novel biomarkers or promising therapeutic targets of human malignant tumors. The association between miR-13p and its target genes may deepen our understanding of the molecular mechanisms contributing to LUAD development, facilitating the discovery of improved therapies for LUAD
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