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"Sometimes I don't have a pulse … and Now i'm still living!Inches Interview using medical professionals to educate yourself regarding their particular activities of as well as views on population-based electronic digital wellbeing systems.
RESULTS XIST and NEK5 were highly expressed while miR-381-3p was lowly expressed in NPC (tissues and cells) and hypoxia-induced NPC cells. Deficiency of XIST or NEK5 suppressed hypoxia-induced glycolysis and metastasis in NPC cells. Moreover, miR-381-3p could directly bind to XIST and its inhibition reversed the inhibitory effects of XIST knockdown on glycolysis and metastasis under hypoxia. NEK5 was a direct target of miR-381-3p and its interference attenuated the promotive effects of miR-381-3p downregulation on glycolysis and metastasis under hypoxic conditions. Besides, interference of XIST decreased tumor growth by upregulating miR-381-3p and downregulating NEK5. CONCLUSIONS XIST knockdown inhibited glycolysis and metastasis in hypoxia-induced NPC cells through regulating miR-381-3p/NEK5 axis, providing new insights into the pathogenesis of NPC.OBJECTIVE Nasopharyngeal carcinoma (NPC) is a malignancy and is prone to distant metastasis and radioresistance. Long non-coding RNAs (lncRNAs) play vital roles in human cancers. The purpose of this study was to explore the role and the action mechanism of intergenic lncRNA (LINC00114) in NPC. MATERIALS AND METHODS The expression of LINC00114 and microRNA-203 (miR-203) was measured by quantitative real-time polymerase chain reaction (qRT-PCR). NPC cells were exposed to X-ray as radiation treatment. Cell proliferation, migration, cell survival fraction and apoptosis were assessed by 3-(4, 5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT), transwell, colony formation, and flow cytometry assays, respectively. The expression of Cleaved-cas-3, Cleaved-cas-9, phosphor-ERK (p-ERK) and phosphor-JNK (p-JNK) was quantified by Western blot. The interaction between miR-203 and LINC00114 was predicted by bioinformatics tool microRNA.org and verified by dual-luciferase reporter assay. Tumor formation assay in nude mice was conducted to examine the role of LINC00114 in vivo. RESULTS LINC00114 was upregulated in serums from NPC patients, tissues and cell lines of NPC. LINC00114 knockdown inhibited proliferation, migration, and radioresistance of NPC cells. MiR-203 was a target of LINC00114, and miR-203 inhibition eliminated the effects of LINC00114 knockdown. Besides, the extracellular signal-regulated kinases (ERK)/c-Jun N-terminal kinases (JNK) pathway was inactivated by LINC00114 knockdown but recovered by miR-203 inhibition. Moreover, LINC00114 knockdown suppressed tumor growth and radioresistance in vivo. CONCLUSIONS LINC00114 contributed to NPC development and radioresistance through the regulation of ERK/JNK signaling pathway and the mediation of miR-203, suggesting that LINC00114 was a promising biomarker to defense NPC progression and radioresistance.OBJECTIVE Previous studies have shown that LINC00657 is a cancer-promoting gene. However, the role of LINC00657 in oral squamous cell carcinoma (OSCC) has not been reported. This study was designed to investigate the role of LINC00657 in OSCC and its regulatory mechanism. PATIENTS AND METHODS Quantitative Real Time-Polymerase Chain Reaction (qPCR) was used to detect the levels of LINC00657 and microRNA-150 in 32 pairs of OSCC tissues and normal ones, and the correlation between LINC00657 and clinical indicators and OSCC patient's prognosis was analyzed. qRT-PCR further verified the levels of LINC00657 and microRNA-150 in OSCC cells. In addition, LINC00657 overexpression and knockdown models were constructed using lentivirus in OSCC cell lines Fadu and Tca8113, and Cell Counting Kit-8 (CCK-8), plate clone experiment, and 5-Ethynyl-2'-deoxyuridine (EdU) assay were carried out to evaluate the influence of LINC00657 on the biological functions of OSCC cells. Further, Luciferase reporter gene and recovery experimeit may accelerate the malignant progression of OSCC via regulating microRNA-150.OBJECTIVE Circular RNAs (circRNAs) play a wide role in human cancers, including oral squamous cell carcinoma (OSCC). The purpose of this study was to investigate the biological functions of circ_0001971 and associated mechanisms in OSCC. MATERIALS AND METHODS The expression of circ_0001971, miR-194, and miR-204 was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Cell proliferation and viability were assessed using cell counting kit-8 (CCK-8) assay. Cell migration and invasion were examined using the transwell assay. Cell apoptosis was monitored by flow cytometry assay. The protein levels of proliferation marker (CyclinD1), epithelial mesenchymal-transition (EMT) markers (E-cadherin (E-cad) and N-cadherin (N-cad)) and apoptosis markers (Cleaved-caspase-3 (Cleaved-cas-3) and Cleaved-caspase-9 (Cleaved-cas-9)) were measured by Western blot. The relationship between circ_0001971 and miR-194 or miR-204 was predicted by online tool starBase and verified by the Dual-Luciferase reporter assay and RNA immunoprecipitation (RIP) assay. Tumor formation assay in nude mice was conducted to observe the role of circ_0001971 in vivo. RESULTS The expression of circ_0001971 was significantly increased in tumor tissues and cell lines. Circ_0001971 knockdown inhibited cell proliferation, migration, and invasion but promoted cisplatin (DDP) sensitivity and cell apoptosis. It was confirmed that miR-194 and miR-204 were targets of circ_0001971, and miR-194 inhibition or miR-204 inhibition reversed the effects of circ_0001971 knockdown in OSCC cells. Moreover, circ_0001971 knockdown impeded tumorigenesis and development in vivo. CONCLUSIONS Circ_0001971 regulates cell proliferation, migration, invasion, apoptosis, and chemosensitivity of OSCC by interacting with miR-194 and miR-204 in vitro and in vivo. We provided a theoretical basis for the action mechanism of circ_0001971 on OSCC progression and chemosensitivity.OBJECTIVE The aim of this study was to investigate the potential role of LINC00511 in esophageal cancer (ECa), and to explore its underlying mechanism through in vitro cell experiments. PATIENTS AND METHODS LINC00511 expression in ECa was analyzed by GEPIA database and verified by real-time fluorescence quantitative polymerase chain reaction (qPCR). The bioinformatics website was used to analyze the miRNAs that can bind to LINC00511, and the regulatory relationship between them was verified through Luciferase assay, qPCR as well as Western blotting analysis. Then, the impacts of LINC00511 and microRNA-150-5p on the proliferation or invasiveness of ECa cell lines Kyse30 and ECA109 were investigated by cell counting kit-8 (CCK-8) test and transwell experiment, respectively. read more Meanwhile, cell cycle and apoptosis were detected by flow cytometry. RESULTS Analysis results of the GEPIA database revealed that LINC00511 had a significant high expression in ECa tissue samples in comparison with normal control ones, which is consistent with qPCR results.
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