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MiRNA-mRNA crosstalk in laryngeal squamous cell carcinoma based on the TCGA database.

The functional characterization of non-coding microRNAs (miRNAs) has been shown to be associated with the pathophysiology of the disease, but it is still a challenging task to elucidate the pathogenesis of microRNAs and disease. In addition, the understanding of the role of miRNAs in the development of LSCC still needs further exploration.

2911 related Products with: MiRNA-mRNA crosstalk in laryngeal squamous cell carcinoma based on the TCGA database.

Lung squamous cell carcin Cervix squamous cell carc Esophagus squamous cell c Esophagus squamous cell c Esophageal squamous cell Esophagus squamous cell c Esophageal squamous cell Laryngeal squamous cell c Oral cavity squamous cell Skin squamous cell carcin Multiple organ squamous c Esophagus squamous cell c

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MicroRNA-193b-3p Regulates Matrix Metalloproteinase 19 Expression in Interleukin-1β-Induced Human Chondrocytes.

Micro(mi)RNAs are small, non-coding RNA molecules known to play a significant role in osteoarthritis (OA) initiation and development, and similar to matrix metalloproteinases (MMPs), they participate in cartilage degeneration and cleave multiple extracellular matrices. The aim of this study was to determine whether the expression of MMP-19 in interleukin (IL)-1β-induced human chondrocytes is directly regulated by miR-193b-3p. Expression levels of miR-193b-3p and MMP-19 in normal and osteoarthritis (OA) human cartilage, and interleukin-1 β (IL-1β)-induced human chondrocytes were determined by real-time polymerase chain reaction. Additionally, expression level of MMP-19 in IL-1β-induced human chondrocytes was estimated by western blotting and immunohistochemistry analyses. The effect of miR-193b-3p on MMP-19 expression was evaluated using transient transfection of normal human chondrocytes with miR-193b-3p mimic or its antisense inhibitor (miR-193b-3p inhibitor), and siMMP-19. The putative binding site of miR-193b-3p in the 3'-untranslated region (UTR) of MMP-19 mRNA was validated by luciferase reporter assay. miR-193b-3p expression was reduced in OA cartilage compared to that in normal chondrocytes, while the opposite was observed for MMP-19. Upregulation of MMP-19 expression was correlated with downregulation of miR-193b-3p in IL-1β-stimulated normal chondrocytes. Increase in miR-193b-3p levels was associated with silencing of MMP-19. Overexpression of miR-193b-3p suppressed the activity of the reporter construct containing the 3'-UTR of human MMP-19 mRNA and inhibited the IL-1β-induced expression of MMP-19 and iNOS in chondrocytes, while treatment with miR-193b-3p inhibitor enhanced MMP-19 expression. MiR-193b-3p is an important regulator of MMP-19 in human chondrocytes and may relieve the inflammatory response in OA. This article is protected by copyright. All rights reserved.

1143 related Products with: MicroRNA-193b-3p Regulates Matrix Metalloproteinase 19 Expression in Interleukin-1β-Induced Human Chondrocytes.

Anti AGO2 Human, Monoclon Anti AGO2 Human, Monoclon Human Interleukin-19 IL-1 Anti AGO2 Mouse, Monoclon Anti AGO2 Mouse, Monoclon CELLKINES Natural Human I Human Interleukin-4 IL-4 Human Interleukin-6 IL-6 Human Interleukin-7 IL-7 Human Interleukin-2 IL-2 Human Interleukin-16 IL-1 Human Interleukin-33 IL-3

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Identification of prognostic signature in cancer based on DNA methylation interaction network.

The identification of prognostic biomarkers for cancer patients is essential for cancer research. These days, DNA methylation has been proved to be associated with cancer prognosis. However, there are few methods which identify the prognostic markers based on DNA methylation data systematically, especially considering the interaction among DNA methylation sites.

2137 related Products with: Identification of prognostic signature in cancer based on DNA methylation interaction network.

DNA (cytosine 5) methyltr removed without changing Cancer Apoptosis Phospho- Top five cancer tissue ar Multiple organ cancer tis Lung cancer tissue array, Lung cancer tissue array Colon cancer and normal t Colon cancer and normal t Colon cancer, metastasize Colon cancer and matched Colon cancer tissue array

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Target gene screening and evaluation of prognostic values in non-small cell lung cancers by bioinformatics analysis.

Non-small cell lung cancer (NSCLC) is the major leading cause of cancer-related deaths worldwide. This study aims to explore molecular mechanism of NSCLC.

2537 related Products with: Target gene screening and evaluation of prognostic values in non-small cell lung cancers by bioinformatics analysis.

Small cell lung carcinoma Non small cell lung carci Non small cell lung carci Lung small cell carcinoma Lung non small cell cance High density non small ce Middle advanced stage lun Multiple lung carcinoma ( Non-small cell lung cance Non small cell lung carci Non small cell lung carci Non small cell lung carci

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MicroRNA-204-3p inhibits lipopolysaccharide-induced cytokines in familial Mediterranean fever via the phosphoinositide 3-kinase γ pathway.

We sought to identify the microRNA (miRNA) profile and potential biomarkers in FMF and to clarify their gene targets to elucidate the pathogenesis of FMF.

1871 related Products with: MicroRNA-204-3p inhibits lipopolysaccharide-induced cytokines in familial Mediterranean fever via the phosphoinositide 3-kinase γ pathway.

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MiR-31a-5p protects myocardial cells against apoptosis by targeting Tp53.

The pathogenesis and progression of heart failure (HF) involves multiple mechanisms, including the increased activity of the renin-angiotensin-aldosterone system, apoptosis and differential expression of microRNAs (miRNAs/miRs). Our previous study revealed an increase in miR‑31a‑5p levels in the failing hearts of a rat HF model. In the present study, whether and how miR‑31a‑5p mediates angiotensin II (AngII)‑induced apoptosis in the cardiac H9C2 cell line, was investigated using molecular biological approaches, including reverse transcription followed by quantitative polymerase chain reaction, western blotting, RNA arrays, and mutagenesis. It was demonstrated that AngII stimulation increased apoptosis and decreased miR‑31a‑5p expression, which coincided with increased tumor protein p53 (Tp53) levels. Overexpression of miR‑31a‑5p significantly suppressed the AngII‑induced apoptotic rate and caspase‑3 activity, while suppression of miR‑31a‑5p did the opposite. A total of 16 proapoptotic genes that were downregulated and 4 antiapoptotic genes that were upregulated in the miR‑31a‑5p‑overexpressed cells were identified. It was also revealed that Tp53 mRNA contained the seed sequence in its 3'‑untranslated region for miR‑31a‑5p binding. The luciferase reporter analysis showed that miR‑31a‑5p repressed the luciferase activity of the wild‑type seed sequence, but not the mutated seed sequence fused to a reporter construct. Thus, it was demonstrated that miR‑31a‑5p mediated AngII‑triggered apoptosis in myocardial cells at least partially through targeting Tp53. These findings advance the understanding of the functional interaction between miRNAs and Tp53 in the setting of cardiac diseases. Further work is required to explore whether miR‑31a‑5p can serve as a therapeutic target for HF treatment in vivo.

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Genetic Variations in the 3'-untranslated Regions of Genes Involved in the Cell Cycle and Apoptosis Pathways Affect Bladder Cancer Risk.

Key genes related to cell cycle and apoptosis pathways play critical roles in bladder cancer. Single nucleotide polymorphisms (SNPs) in the 3'-untranslated regions (3'-UTR) of genes may impact microRNA (miRNA)-messenger RNA (mRNA) binding capacity and alter gene expression to contribute to the susceptibility of cancers. However, an association of genetic variations in cell cycle and apoptosis pathways with bladder cancer risk, has not been reported.

2993 related Products with: Genetic Variations in the 3'-untranslated Regions of Genes Involved in the Cell Cycle and Apoptosis Pathways Affect Bladder Cancer Risk.

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Control the intracellular NF-κB activity by a sensor consisting of miRNA and decoy.

Many diseases are associated with the abnormal activation of NF-κB and its signaling pathway. NF-κB has become an important target for disease treatment and development of new drugs. Many various NF-κB inhibitors were therefore developed; however, they have difficulties to become clinical drugs due to their adverse side effects resulted from the affected normal physiological functions of this transcription factor. To overcome this limitation, this study construct a transgenic vector that can express an artificial miRNA targeting NF-κB RelA under the control of a NF-κB-specific promoter. The promoter consists of a NF-κB decoy and a minimal promoter. The vector was named as decoy minimal promoter-artificial microRNA (DMP-amiRNA). This study verified that this vector can sense and control the intracellular NF-κB activity upon transfection. Working of the vector forms a perfect feedback loop that realizes the NF-κB self-control. With the vector in cells, the higher NF-κB activity, the higher DMP transcriptional activity, and the more amiR533 expression. DMP-amiRNA can moderately inhibit the intracellular NF-κB activity but exert no significant effect on cell viability. This study therefore develops a new strategy for inhibiting over activity of NF-κB, which should has great potential in clinical application.

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Mutant Runx2 regulates amelogenesis and osteogenesis through a miR-185-5p-Dlx2 axis.

Regulation of microRNAs (miRNA) has been extensively investigated in diseases; however, little is known about the roles of miRNAs in cleidocranial dysplasia (CCD). The aim of the present study was to investigate the potential involvement of miRNAs in CCD. In vitro site-directed mutagenesis was performed to construct three mutant Runx2 expression vectors, which were then transfected into LS8 cells and MC3T3-E1 cells, to determine the impact on amelogenesis and osteogenesis, respectively. miRCURY LNA miRNA microarray identify miR-185-5p as a miRNA target commonly induced by all three Runx2 mutants. Real-time quantitative PCR was applied to determine the expression of miR-185-5p and Dlx2 in samples. Dual-luciferase reporter assays were conducted to confirm Dlx2 as a legitimate target of miR-185-5p. The suppressive effect of miR-185-5p on amelogenesis and osteogenesis of miR-185-5p was evaluated by RT-PCR and western blot examination of Amelx, Enam, Klk4, and Mmp20 gene and protein expression, and by Alizarin Red stain. We found that mutant Runx2 suppressed amelogenesis and osteogenesis. miR-185-5p, induced by Runx2, suppressed amelogenesis and osteogenesis. Furthermore, we identified Dlx2 as direct target of miR-185-5p. Consistently, Dlx2 expression was inversely correlated with miR-185-5p levels. This study highlights the molecular etiology and significance of miR-185-5p in CCD, and suggests that targeting miR-185-5p may represent a new therapeutic strategy in prevention or intervention of CCD.

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G(s) Alpha subunit (Mutan Androgen Receptor (Phosph Androgen Receptor (Phosph Rabbit Anti-Human Androge Rabbit Anti-Human Androge Androgen Receptor (Ab 650 Recombinant Human TNF-alp Recombinant Human TNF-alp Recombinant Human TNF-alp AZD-3514 Mechanisms: Andr 17β-Acetoxy-2α-bromo-5 (5α,16β)-N-Acetyl-16-[2

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MicroRNA-92a-3p Regulates Aggrecanase-1 and Aggrecanase-2 Expression in Chondrogenesis and IL-1β-Induced Catabolism in Human Articular Chondrocytes.

Aggrecanase-1 (ADAMTS-4) and aggrecanase-2 (ADAMTS-5) are secreted enzymes belonging to the ADAMTS (a disintegrin and metalloproteinase with thrombospondin motifs) family that play significant roles in the progression of osteoarthritis (OA). Here, we aimed to determine whether the expression of ADAMTS-4/5 in chondrogenesis and inflammation is regulated by microRNA-92a-3p (miR-92a-3p).

2517 related Products with: MicroRNA-92a-3p Regulates Aggrecanase-1 and Aggrecanase-2 Expression in Chondrogenesis and IL-1β-Induced Catabolism in Human Articular Chondrocytes.

Anti AGO2 Human, Monoclon Human Interleukin-16 IL-1 Human Interleukin-17E (IL Human Epstein-Barr Virus Human Interleukin-1-alpha Human Interleukin-10 IL-1 Human Interleukin-11 IL-1 Human Interleukin-13 IL-1 Human Interleukin-15 IL-1 Human Interleukin-19 IL-1 Human Interleukin-21 IL-2 Recombinant Human Interle

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