IC50 of Geneticin (G418) antibiotic was measured using MTT test in NSCLC cell lines. miR-145 was transfected into lung cancer cells by jetPEI. qRT-PCR was used to evaluate the transcript level of the miR-145 and expression for KRAS, MMP-9, vimentin, caspase-3, caspase-8 and caspase-9 genes in A549 cells.
Mechanistically, JPX upregulates cyclin D2(CCND2) expression in a competing endogenous RNA mechanism by interacting with miR-145-5p, thus provoking the development and progression of NSCLC.
With good sensitivity and specificity of single miR-197 and single miR-145 for the diagnosis of NSCLC, the combined detection of miR-197 and miR-145 can achieve a better sensitivity in the diagnosis of NSCLC.
The present study investigated the effects of miR-145 on the proliferation, invasion, metastasis and apoptosis of the NSCLC A549 cell line and the underlying molecular mechanism of its action.
The protein expression of Bax, epidermal growth factor receptor (EGFR), phosphatidylinositol 3‑kinase (PI3K) and phosphorylated‑protein kinase B (AKT) was examined by western blot analysis. miR‑145 expression was downregulated in patients with NSCLC who were treated with chemotherapy.
The tumor suppressor miR‑145 has been reported to be lowly expressed in numerous types of human cancer; in the present study, the expression levels of miR‑145 were decreased in patients with NSCLC.
Here, qRT-PCR analysis revealed that p53 and ROR were upregulated while miR-145 was downregulated in non-small cell lung cancer (NSCLC) tissues and LCSCs compared to their paired adjacent normal tissues and lung cancer cells (LCCs).
MiR-145 expression in NSCLC tissues was lower than that in adjacent normal tissues, while mTOR expression was higher in NSCLC tissues than in adjacent normal tissues.
These results show a novel association between miR-21, miR-376c and miR-145 and their host target genes with the presence of MCPyV, suggesting a mechanism of virus-specific microRNA signature in NSCLC.
However, the mechanistic role of miR-203 and miR-145 in TGF-β-induced epithelial-mesenchymal transition (EMT) has not yet been elucidated in human cancers, including NSCLC.
In addition, AEG-1/MTDH was a direct target of miR-145, and the expression of AEG-1/MTDH was inversely correlated with miR-145 expression in NSCLC tissues.
Here we show that miR-145 was down-regulated in NSCLC tissues; down-regulation of miR-145 was correlated with late clinical stage and poorly differentiated carcinoma, and, low expression level of miR-145 could also predict chemotherapy resistance and shorter disease-free survival (DFS).
The purpose of this study was to evaluate whether circulating miR-125a-5p, miR-145 and miR-146a could be used as biomarkers for the diagnosis of NSCLC through measuring their expression and assess their relationship with clinical pathological factors.