Circ_0007385 promotes the proliferation and inhibits the apoptosis of non-small cell lung cancer cells via miR-337-3p-dependent regulation of LMO3.

BACKGROUND: This study intended to analyze the expression characteristic, functions and underlying mechanism of circular RNA_0007385 (circ_0007385) in non-small cell lung cancer (NSCLC). METHODS AND RESULTS: RNA and protein expression was examined by real-time quantitative polymerase chain reaction (RT-qPCR) and Western blot assay. Cell counting kit 8 (CCK8) assay, colony formation assay, 5-Ethynyl-2'-deoxyuridine (EdU) assay and flow cytometry were applied to analyze cell proliferation ability. Flow cytometry was also conducted to assess cell apoptosis. Dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay were performed to verify the predicted target relationships. Xenograft tumor model was utilized to analyze the function of circ_0007385 in vivo, and immunohistochemistry (IHC) assay was used to analyze protein expression in xenograft tumor tissues. Circ_0007385 expression was notably enhanced in NSCLC tissues and cell lines. Circ_0007385 facilitated the proliferation but suppressed the apoptosis of NSCLC cells. Circ_0007385 acted as a sponge for microRNA-337-3p (miR-337-3p), and circ_0007385 overexpression-mediated effects were largely overturned by the overexpression of miR-337-3p in NSCLC cells. MiR-337-3p interacted with the 3' untranslated region (3'UTR) of LIM-only protein 3 (LMO3). Circ_0007385 up-regulated LMO3 level by absorbing miR-337-3p in NSCLC cells. LMO3 overexpression largely reversed miR-337-3p overexpression-induced influences in NSCLC cells. Circ_0007385 knockdown significantly restrained the growth of xenograft tumors in vivo. CONCLUSION: Circ_0007385 promoted the proliferation ability and inhibited the apoptosis of NSCLC cells by binding to miR-337-3p to induce LMO3 expression.

miR-130a-Mediated KLF3 Can Inhibit the Growth of Lung Cancer Cells.

BACKGROUND: The 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. METHODS: Quantitative 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. RESULTS: miR-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. CONCLUSION: miR-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.