Abstract
BackgroundMetastasis and disease refractoriness remain as major challenges for non-small cell lung cancer (NSCLC) treatment and understanding the underlying molecular mechanisms is of scientific and clinical value. Therefore, in this study, we aimed to explore the effects of circMED13L_012 on the proliferation, migration, invasion and drug-resistance of NSCLC tumor cells.MethodsIn this study, we utilized clinical samples and NSCLC cell lines to explore the association between circMED13L_012 expressions and tumor cell metastasis and chemo resistance. CCK8 and transwell assay were conducted to explore the impact of circMED13_012 on NSCLC tumor proliferation and migrative capabilities. Dual-luciferase reporter gene assay was conducted to validate the circMED13L_012 interaction network.ResultsOur results demonstrated that circMED13L_012 exhibited significantly elevated average level in our clinical samples of NSCLC, compared with normal tissues. circMED13L_012 level was positively correlated with disease stage and metastatic status. Increased circMED13L_012 expression was associated with the enhanced migration, proliferation and chemo resistance of NSCLC cell lines. Further experiments indicated that circMED13L_012 promoted malignant behavior of NSCLC tumor cells by targeting MAPK8 through modulation miR-433-3p expression.ConclusionsOur study for the first time demonstrated that circMED13L_012–miR-433-3p–MAPK8 axis played important role for NSCLC pathogenesis, which could be potential therapeutic target for the development of future NSCLC treatment.
Highlights
Metastasis and disease refractoriness remain as major challenges for non-small cell lung cancer (NSCLC) treatment and understanding the underlying molecular mechanisms is of scientific and clinical value
Another research demonstrated that tumor epithelial to mesenchymal transition (EMT) process was closely associated with circRNAs biogenesis [10], which indicating potential roles of circRNAs in tumor metastasis
Further experiments using actinomycin D, which is a transcription inhibitor, indicated that circMED13L_012 circular transcripts were more stable compared with linear transcripts of MED13L mRNA (Fig. 1c)
Summary
Metastasis and disease refractoriness remain as major challenges for non-small cell lung cancer (NSCLC) treatment and understanding the underlying molecular mechanisms is of scientific and clinical value. In this study, we aimed to explore the effects of circMED13L_012 on the proliferation, migration, invasion and drug-resistance of NSCLC tumor cells. Another research demonstrated that tumor epithelial to mesenchymal transition (EMT) process was closely associated with circRNAs biogenesis [10], which indicating potential roles of circRNAs in tumor metastasis. Up till the exact role of circMED13_012 in lung cancer pathogenesis and disease progression remains undiscovered. In this study, we aimed to evaluate the molecular impact of circMED13_012 on lung cancer cells and further explore the gene regulatory network of circMED13_012 for NSCLC
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