Effects of miR‑218‑1‑3p and miR‑149 on proliferation and apoptosis of non‑small cell lung cancer cells

Abstract

The aim of the present study was to explore the effects of miR-218-1-3p and miR-149 on the biological function of non-small cell lung cancer (NSCLC) cells A549. Paired NSCLC and adjacent tissues were obtained from 50 NSCLC patients admitted to Shandong Provincial Chest Hospital Affiliated to Shandong University (Jinan, China) from April 2015 to May 2018. The expression levels of miR-218-1-3p and miR-149 were detected by reverse transcription-quantitative PCR (RT-qPCR). The lung adenocarcinoma A549 cells were assigned into the blank group (without transfection), negative control (NC) group (transfected with miRNA NC), and the transfected groups miR-218-1-3p mimic and miR-149 mimic groups. Proliferation and cell growth were determined by CCK-8 assay and cell invasion ability in vitro was assessed by Transwell assay. Flow cytometry was carried out for the detection of cell apoptosis. RT-qPCR results showed that the expression levels of miR-218-1-3p and miR-149 in NSCLC tissues were significantly lower than those in adjacent tissues (P<0.001). At 48 and 72 h, the cell growth of the A549 cells in the miR-218-1-3p mimic and miR-149 mimic groups was significantly lower than that in the NC and blank groups (P<0.05). The number of invasive cells in the miR-218-1-3p mimic and miR-149 mimic groups was significantly lower than that in the NC and blank groups (P<0.05). The apoptotic rate of A549 cells in the miR-218-1-3p mimic and miR-149 mimic groups was significantly higher than that in the NC and blank groups (P<0.05). In conclusion, upregulation of miR-218-1-3p and miR-149 can inhibit the proliferation, invasion and migration of A549 cells in NSCLC, thereby promoting the apoptosis of A549 cells. Thus, miR-218-1-3p and miR-149 can be used as new molecular targets for the diagnosis and treatment of NSCLC.

Cathepsin-facilitated invasion of BMI1-high hepatocellular carcinoma cells drives bile duct tumor thrombi formation

“…Importantly, our data illustrate that overexpression of miR-218-1-3p inhibits CTSB secretion in BMI1 expressing cells, while its expression also affects their invasion and trans-intrahepatic biliary epithelial migration ability. In support of this finding, Guo et al shows that miR-218-1-3p regulates lung cancer cell invasiveness 41 , while its expression has been linked with epithelial mesenchymal transition and angiogenesis in colorectal cancer 42 . We also discover that miR-218-1-3p overexpression reduces jaundice, gall bladder and bile duct enlargement and BDTT in WB BMI1 implanted mice, independent of primary orthotopic liver tumor growth.…”

PI3K/AKT pathway‐related microRNA variants in childhood acute lymphoblastic leukemia

“…miR-149 is a well-known tumor regulator that is dysregulated in various cancers, including oral squamous cell carcinoma, digestive system cancers, and lung cancer. [20][21][22] Several target genes of miR-149 have been identified, including FASLG, caspase-2, AKT1, PARP-2, and FOXM1. 23 In previous research, miRNA-149 was found to be an oncogenic regulator in ALL.…”

MicroRNAs in Body Fluids: A More Promising Biomarker for Clear Cell Renal Cell Carcinoma

“…93 Guo et al found that miR-149 strongly inhibited the growth of nonsmall cell lung cancer (NSCLC) and promoted its apoptosis. 94 However, Xiao et al gave a different evidence that exosomal miR-92a-1-5p was down-regulated while exosomal miR-424-3p and miR-149-3p were significantly up-regulated in RCC. 87 MiRNAs could play an opposite role in different cancers, but it is thought-provoking that there are differences in expression patterns between exosomes and cell lines of the same cancer.…”