Abstract
BackgroundThe role of microRNA (miR) in tumors has been reported in numerous articles. Previous studies have found that miR-130a is low expressed in lung cancer, but the related mechanism has not been fully elucidated. This study mainly explores the mechanism of miR-130a in lung cancer, so as to provide potential therapeutic targets for clinical applications.MethodsQuantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the expression of miR-130a and KLF3 in the tissues of lung cancer patients. The miR-130a-mimics and miR-130a-inhibit were constructed. Cell proliferation, invasion, migration and apoptosis were determined by CCK-8, transwell, scratch test and flow cytometry. Western Blot was used to determine the expression of KLF3 protein in cells, and the dual-luciferase reporter to determine the relationship between KLF3 and miR-130a.ResultsmiR-130a shows low expression in NSCLC patients, while KLF3 shows high expression, exhibiting a negative correlation. The 5-year survival rate of patients with low miR-130a expression and high KLF3 expression was reduced. Cox regression analysis showed that miR-130a was an independent prognostic factor for NSCLC patients. The dual-luciferase reporter revealed that miR-130a bound to KLF3 in a targeted manner, and cell experiments showed that miR-130a could inhibit the growth of lung cancer cells by regulating the expression of KLF3.ConclusionmiR-130a shows low expression in lung cancer and predicts a poor prognosis. In addition, up-regulation of miR-130a can down-regulate KLF3 and inhibit the growth of lung cancer.
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