The present study aimed to investigate the expression of microRNA-495 (miR-495) in non-small cell lung cancer (NSCLC) tissues and cells, as well as its function on the proliferation of lung cancer cells. The expression of miR-495 in 122 pairs of NSCLC tissues and matched paracarcinoma tissues, as well as in human lung cancer cell lines (A549, H460, H1650, H520 and SK-MES-1) and the normal human pulmonary bronchial epithelial cell line 16HBE was determined using reverse transcription quantitative polymerase chain reaction (RT-qPCR). As predicted by bioinformatics analysis, high mobility group A2 (HMGA2) may be a potential target gene of miR-495. In addition, the regulatory function of miR-495 on its target gene HMGA2 was evaluated using a dual-luciferase reporter assay, RT-qPCR and western blotting. Furthermore, the effect of miR-495 on the proliferation of A549 lung cancer cells was investigated using a Cell Counting Kit-8 (CCK-8) assay. The results demonstrated that the expression of miR-495 in NSCLC tissues and cells was significantly downregulated compared with the control. In addition, downregulated expression of miR-495 was associated with tumor differentiation, lymph node metastasis and tumor, node and metastasis staging. Additionally, a dual-luciferase reporter assay revealed that miR-495 could directly associated with the 3′-untranslated region of HMGA2. Upregulated expression of miR-495 significantly downregulated the mRNA and protein expression levels of HMGA2 in A549 cells. Furthermore, the results of CCK-8 assay revealed that upregulated expression of miR-495 significantly suppressed the proliferation of A549 cells; HMGA2 overexpression reversed this inhibition. In summary, the findings of the present study demonstrated that miR-495 was downregulated in NSCLC tissues and cells. In addition, miR-495 suppressed the proliferation of lung cancer cells by directly targeting HMGA2.
The present study aimed to examine microRNA (miR)-940 expression in esophageal squamous cell carcinoma (ESCC) tissues and cells, analyze its association with the clinicopathological features and prognosis of patients, and explore the potential underlying mechanisms. miR-940 expression in ESCC cell lines and a normal esophageal cell line was detected using reverse transcription-quantitative (RT-q)PCR. Furthermore, 210 resected ESCC tissue and para-carcinoma tissue specimens were collected, and miR-940 expression in those tissues was detected by RT-qPCR. In addition, the association of miR-940 with the clinicopathological features and prognosis of patients was analyzed. In an in vitro experiment, miR-940 mimics were transduced into ESCC cells by the liposome method. An MTT assay was used to detect the effect of miR-940 on the viability of ESCC cells. The influence of miR-940 on the cell cycle and apoptotic rate of ESCC cells was detected by flow cytometry. The present results indicated that the expression levels of miR-940 in human ESCC tissues and cell lines were markedly downregulated, and that low expression of miR-940 in ESCC tissues was significantly associated with a poor degree of differentiation, positive lymph node metastasis and advanced clinical stage. Kaplan-Meier survival analysis suggested that low miR-940 expression was associated with poor prognosis. Cox regression analysis revealed that lymph node metastasis, clinical stage and miR-940 expression were independent risk factors affecting the prognosis of patients. Overexpression of miR-940 in ESCC cells markedly reduced the cell viability, blocked the cell cycle at G0/G1 phase and promoted cell apoptosis. These results suggest that miR-940 is downregulated in ESCC, which is linked to the occurrence and progression of ESCC. Conversely, overexpression of miR-940 reduced the cell viability and promoted apoptosis of ESCC cells. Therefore, miR-940 may be a promising novel prognostic marker and anti-cancer target in ESCC.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.