Mccormickahmad6725

Dual-Luciferase assay was conducted to detect the ability of miR-449b-5p to regulate the 3'UTR (untranslated regions) of WNT2B. TOP/FOP ratio was used to evaluate the activity of Wnt/β-catenin signaling pathway. Results Down-regulation of miR-449b-5p expression was found in both human glioblastoma tissues and cell lines, which was negatively associated with the clinical stages. Up-regulation of miR-449b-5p inhibited tumor spheres formation, cell viability and proliferation ability of glioblastoma cells. The expression levels of WNT2B and nuclear β-catenin were negatively associated with miR-449b-5p levels in glioblastoma cells. MiR-449b-5p inhibited Wnt/β-catenin signaling by targeting WNT2B. Conclusions MiR-449b-5p acts as a tumor suppressor and retards the oncogenesis of glioblastoma, which is achieved via inactivation of Wnt/β-catenin signaling by directly targeting WNT2B.Objective Glioma is a highly aggressive and lethal brain tumor. Anesthetics have been shown to have important effects on the biological characteristics of cancer cells. Nevertheless, the molecular mechanism of anesthetic-mediated glioma cells progression remains unclear. Materials and methods Sevoflurane (sev) was employed to treat glioma cells. The biological characteristics (viability, colony formation, apoptosis, cell cycle, migration, and invasion) of glioma cells were determined via Cell Counting Kit-8 (CCK-8), cell colony formation, flow cytometry, PI cytometry, or transwell assays. The protein levels of Cell Cycle Dependent Kinase (CDK) 2, CDK4, E-cadherin, N-cadherin, Vimentin, and Transforming Growth Factor Beta (TGFB) induced factor homeobox 2 (TGIF2) were assessed through Western blot analysis. Glucose consumption and lactate production were measured using special commercial kits. The expression of circular RNA has_circ_0012129 (circ_0012129) and miR-761 was detected via quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The relationship between circ_0012129 or TGIF2 and miR-761 was verified with Dual-Luciferase reporter assay. Sevoflurane-mediated molecular mechanisms have been confirmed via xenograft assay. Results Sevoflurane suppressed viability, colony formation, cell cycle, migration, and invasion and promoted apoptosis of glioma cells in vitro, and impeded tumor growth in vivo. Circ_0012129 and TGIF2 were downregulated and miR-761 was upregulated in sevoflurane-treated glioma cells. Circ_0012129 elevation abolished sevoflurane-mediated biological characteristics of glioma cells. MiR-761 served as target for circ_0012129 and miR-761 targeted TGIF2. Moreover, both miR-761 overexpression and TGIF2 suppression restored circ_0012129 enhancement-mediated biological characteristics of sevoflurane-treated glioma cells. Conclusions Sevoflurane mediated the progression of glioma via regulating the circ_0012129/miR-761/TGIF2 axis.Objective Neuroblastoma is the most frequent tumor of sympathetic nervous system in infants. MiRNAs acted as oncogenes or tumor suppressors in the process of tumor development. We aim at exploring the functions of miRNA in neuroblastoma. Patients and methods Cell viability and invasion were evaluated by Cell Counting Kit-8 (CCK-8) and transwell assays. Western blot was utilized to assess the protein expression associated with epithelial-mesenchymal transition (EMT) markers. Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was performed to calculate the mRNA levels of miRNA and gene. Results MiR-424 was downregulated while doublecortin like kinase 1 (DCLK1) was upregulated in neuroblastoma tissues and cells compared to adjacent non-tumor and normal spongiocyte cells. MiR-424 suppressed cell viability, invasion, and EMT by targeting DCLK1. MiR-424 regulated the expression of DCLK1 by directly binding to the 3'-untranslated region (UTR) of DCLK1 mRNA in SK-N-SH and Be2C cells. DCLK1 reversed partial functions of miR-424 in neuroblastoma. Conclusions MiR-424 suppressed cell viability, invasion, and EMT by directly targeting the 3'-UTR of DCLK1 mRNA. The newly identified miR-424/DCLK1 axis provides novel insights into the pathogenesis of neuroblastoma.Objective To investigate the potential effects of miR-200c on proliferation and apoptosis of papillary thyroid cancer (PTC) cells. Materials and methods Micro ribonucleic acid-200c (miR-200c) inhibitor was transfected to down-regulate miR-200c expression. Cell counting kit-8 (CCK-8), colony formation experiment, and flow cytometry were used to detect the effects of miR-200c knockdown on proliferation and apoptosis of Butylated Hydroxytoluene 101 (BHT101) cells. The dual-luciferase reporter gene assay was conducted to detect whether miR-200c directly binds to the target gene. After knocking down miR-200c, quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and Western blotting analysis were performed to detect changes of target genes regarding messenger RNA (mRNA) and protein. Western blotting analysis was also adopted to detect gene expression of Wnt/β-catenin signaling pathway-related proteins. read more Results Compared with those in control group, the proliferation and clone formation ability of BHT101 cells in miR-200c knockdown group were significantly inhibited (p less then 0.05), while the apoptosis rate increased markedly (p less then 0.05). Dachshund Family Transcription Factor 1 (DACH1) was the direct target gene of miR-200c. After miR-200c knockdown, the expression levels of Wnt/β-catenin signaling pathway members (including c-Myc, β catenin and cyclin D1) all decreased. Conclusions MiR-200c is a tumor suppressor miRNA, which promotes proliferation of PTC cells and activates Wnt/β-catenin signaling pathway by directly regulating the corresponding target protein, DACH1.Objective The purpose of this study was to detect the expression of long non-coding ribonucleic acid 00163 (LINC00163) in human papillary thyroid cancer (PTC), and to observe the influence of downregulated LINC00163 on the proliferative and metastatic capacities of human PTC cells. Patients and methods Quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR) assay was applied to measure the expression level of LINC00163 in PTC tissues and para-carcinoma tissues, as well as that in normal human thyroid cells (Nthy-ori3-1) and PTC cells. After the expression of LINC00163 in PTC cells was interfered, qRT-PCR assay was performed to determine the interference efficiency, and colony formation and Cell Counting Kit-8 (CCK-8) assays were conducted to study the impacts of small interfering (si)-LINC00163 on the proliferative capacity of PTC cells. Moreover, wound healing and transwell assays were adopted to investigate the changes in the migratory and invasive abilities of PTC cells after the interference in the expression of LINC00163 in PTC cells.