KLF9 was confirmed to be the direct target of miRNA-20a-5p. There was a negative correlation between the expression levels of miRNA-20a-5p and KLF9 in NSCLC tissues. In addition, KLF9 overexpression could reverse the promotive effects of upregulated miRNA-20a-5p on the proliferation and invasiveness of A549 cells. On the contrary, the knockdown of KLF9 reversed the inhibitory effects of downregulated miRNA-20a-5p on cellular behaviors of PC9 cells. CONCLUSIONS MiRNA-20a-5p stimulates NSCLC to proliferate and invade by targeting KLF9.OBJECTIVE Lung cancer has an unfavorable prognosis due to the lack of efficient diagnostic and therapeutic strategies. Therefore, this study sought to figure out the effect of long non-coding RNA (lncRNA) DANCR on lung cancer progression. PATIENTS AND METHODS LncRNA DANCR and miR-214-5p expressions in non-small cell lung cancer (NSCLC) were detected by Real Time-quantitative Polymerase Chain Reaction (RT-qPCR). Function assays, including Cell Counting Kit-8 (CCK-8) and flow cytometric analysis were conducted to clarify the role of DANCR and miR-214-5p in the progression of NSCLC. Western blot, Dual-Luciferase reporter assay, and RNA immunoprecipitation assay (RIP) were performed to elucidate the underlying mechanism. RESULTS LncRNA DANCR was upregulated in NSCLC. The knockdown of lncRNA DANCR inhibited cell proliferation and accelerated cell apoptosis in NSCLC. LncRNA DANCR interacted with miR-214-5p. MiR-214-5p over-expression partially reversed the regulatory effects of DANCR on proliferation and apoptosis in NSCLC. In addition, CIZ1 was the downstream gene binding miR-214-5p. LncRNA DANCR could regulate the miR-214-5p/CIZ1 axis. CONCLUSIONS Downregulation of lncRNA DANCR inhibited cell proliferation and induced cell apoptosis in NSCLC by regulating the miR-214-5p/CIZ1 axis. LncRNA DANCR may act as an oncogene and promote the progression of NSCLC.OBJECTIVE The present study aimed to determine the expression of long non-coding RNA (lncRNA) FOXD3 antisense RNA 1 (FOXD3-AS1) in lung cancer tissues and to explore its underlying mechanisms in mediating non-small cell lung cancer (NSCLC) progression. MATERIALS AND METHODS Gene expression levels were determined by quantitative real-time PCR; lung cancer cell proliferation and invasion were determined by in vitro functional assays; protein levels were determined by Western blot assay; xenograft nude mice model was used to evaluate the in vivo tumor growth of lung cancer cells; Luciferase reporter assay determined the interactions among FOXD3-AS1, miR-127-3p, and mediator complex subunit 28 (MED28). RESULTS Data mining and analysis of the clinical sample showed that FOXD3-AS1 expression was significantly up-regulated in lung cancer tissues. In vitro functional assays demonstrated that FOXD3-AS1 overexpression promoted NSCLC cell proliferation and invasion, while FOXD3-AS1 knockdown exerted tumor-suppressive effects on NSCLC cells. Moreover, FOXD3-AS1 interacted with miR-127-3p by acting as a competing endogenous RNA to suppress miR-127-3p expression, while miR-127-3p repressed MED28 expression by targeting MED28 3' untranslated region in NSCLC cells. Mechanistically, the oncogenic effects of FOXD3-AS1 overexpression were significantly attenuated by miR-127-3p overexpression and MED28 knockdown in NSCLC cells. In the xenograft mice model, FOXD3-AS1 knockdown suppressed in vivo tumor growth of A549 cells, and also up-regulated miR-127-3p expression and repressed MED28 expression in the xenograft tumors. In the clinical aspect, the downregulation of miR-127-3p and up-regulation of MED28 were respectively detected in lung cancer tissues. CONCLUSIONS Our findings provided new evidence that the FOXD3-AS1 regulated NSCLC progression via targeting the miR-127-3p/MED28 axis.OBJECTIVE Recent researches have proved that circular RNAs (circRNAs) act as an important role in many diseases. Our study aims to uncover the role of circ-ABCB10 in the progression of non-small cell lung cancer (NSCLC). PATIENTS AND METHODS Real Time-quantitative Polymerase Chain Reaction (RT-qPCR) was utilized to detect circ-ABCB10 expression in NSCLC patients. Then, we conducted Cell Counting Kit-8 (CCK-8) assay, colony formation assay, Ethynyl deoxyuridine (EdU) incorporation assay, cell cycle assay, and cell apoptosis assay in treated NSCLC cells. Besides, further experiments including RT-qPCR and Western blot assay were performed to explore the potential mechanism in vitro. RESULTS Circ-ABCB10 expression level was significantly higher in NSCLC samples comparing to that in adjacent tissues. Moreover, functional assays showed that the cell growth ability of NSCLC cells was inhibited after circ-ABCB10 was knocked down. In addition, the cell apoptosis of NSCLC cells was promoted after circ-ABCB10 was knocked down. AD80 c-RET inhibitor Also the expression of KISS1 was upregulated by the knockdown of circ-ABCB10. Furthermore, it was found that KISS1 expression was negatively correlated to the circ-ABCB10 expression in NSCLC tissues. CONCLUSIONS Results above indicated that circ-ABCB10 promoted cell proliferation and inhibited cell apoptosis of NSCLC by suppressing KISS1, which suggested that circ-ABCB10 may be a potential therapeutic target in NSCLC.OBJECTIVE Hypoxia is an important feature of nasopharyngeal carcinoma (NPC). Growing evidence demonstrated that long non-coding RNAs (lncRNAs) could participate in cancer progression and hypoxia regulation. However, the exact roles and underlying mechanism of lncRNA X-inactive specific transcript (XIST) in NPC under hypoxia are still unclear. MATERIALS AND METHODS The expressions of XIST, microRNA-381-3p (miR-381-3p) and NIMA related kinase 5 (NEK5) were detected by quantitative Real-time polymerase chain reaction (qRT-PCR). The glucose consumption and lactate production were measured using the glucose assay kit and lactate assay kit, respectively. Western blot assay was used to determine the protein levels of hexokinase II (HK2) and NEK5. Transwell assay was employed to evaluate cell migration and invasion. The interaction between miR-381-3p and XIST or NEK5 was predicted by bioinformatics analysis and verified by dual-luciferase reporter assay. The mice xenograft model was established to investigate the roles of XIST in NPC progression in vivo.