Thus, the aim of this study is to evaluate the expression level of miR-145-3p which is a shared potential biomarker identified by meta-analysis of breast, prostate and lung cancer data sets.
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.
Logistic regression analysis was conducted to assess the association between polymorphisms in the promoter of miR-143/miR-145 and risk of lung cancer females.
For PFS, the pooled results also showed that the downregulation of miR-145 was significantly associated with poor PFS in patients with multiple tumors (HR = 1.39; 95% CI, 1.16-1.67; <i>P</i> < 0.001), and the subgroup analyses further identified that the low miR-145 expression was associated with worse PFS in patients with lung cancer (HR = 1.97; 95% CI, 1.25-3.09; <i>P</i> = 0.003) and those of Asian descent (HR = 1.50; 95% CI, 1.23-1.82; <i>P</i> < 0.001).
However, the interaction of ROR, p53 and miR-145 in lung cancer and its correlation with lung cancer stem cell (LCSC) signatures were not fully understood.
This prompts for further studies on the mechanisms behind the TP53-induced regulation of SOX2 expression and the possible importance of hsa-miR-145 in lung cancer.
To the best of our knowledge, the results of the present study demonstrated for the first time, that miR‑145 inhibited lung cancer cell metastasis and EMT via targeting the Oct4 mediated Wnt/β‑catenin signaling pathway.
Subsequently, the regulation of miR-145-5p/-3p in the FOXM1signaling pathway was validated by a cohort of 104 matched miRNA and protein (reverse-phase protein array) expression profiles in lung cancer.
These findings establish EGFR and miR-145 links in lung cancer cells and therefore contribute to a better understanding of the role of EGFR in lung cancer cells, and provide clues for in-depth study of miR-145 expression and a possible direction for the further increase of miR-145 in lung cancer cells.
Using quantitative reverse transcriptase PCR analysis, we first selected and identified three aberrant plasma expression miRNAs (miR-21, miR-145, and miR-155) in a training set of 62 patients and 60 healthy smokers to define a panel that had high diagnostic efficiency for lung cancer.
We incorporated 4 copies of miRNA-145 target sequences into the 3'-untranslated region of an HSV-1 essential viral gene, ICP27, to create AP27i145 amplicon viruses and tested their target specificity and toxicity on normal cells and lung cancer cells in vitro.
We, therefore, confirmed that miR-145 can impair the proliferation of human lung adenocarcinoma-initiating cells by targeting OCT4 and leads to inhibition of lung cancer development.