To study the mechanism of BIP regulation gene in 143B cells using RNA-seq Analysis
Ontology highlight
ABSTRACT: RNA-seq has developed to study the gene regulation mechanism. The goals of this study are to investigate the regulated potential genes of BIP.
Project description:The goals of this study are to investigate the molecular mechanism and biomarker by DNA methylation profiles in patients with metabolic syndrome compared to normal.
Project description:This study focused on the key nodes, molecular events and regulatory mechanisms of intestinal microecological disorders that affect the malignant transformation of intestinal epithelial cells into tumors during the occurrence and development of colorectal cancer.
Project description:MiRNAs are important negative regulators of protein coding gene expression, and have been studied intensively over the last few years. Several measurement platforms, designed to determine their relative RNA abundance levels in biological samples, have been developed. In this study, we systematically compared 12 commercially available miRNA expression platforms by measuring an identical set of 20 standardized positive and negative control samples, including human universal reference RNA, human brain RNA and titrations thereof, human serum samples, and synthetic spikes from miRNA family members with varying homology. We developed novel and robust quality metrics to objectively assess platform performance of very different technologies such as small RNA sequencing, RT-qPCR and (microarray) hybridization. We assessed reproducibility, sensitivity, accuracy, specificity, and concordance of differential expression. The results indicate that each method has its strengths and weaknesses, which helps to guide informed selection of a quantitative miRNA gene expression platform in function of particular study goals. Sequencing of 20 miRQC samples on Illumina Genome Analyzer IIx System
Project description:Pulmonary metastasis is the main cause of medical failure and death of osteosarcoma patients. Our recent study identified IRX1 as a potential metastasis-driving gene in osteosarcoma. Studies showed that IRX1 can promote the migration, invasion and anoikis resistance of osteosarcoma cells. We generated 143B stable IRX1 knockdown and control cell lines, and found that IRX1 knockdown can inhibit the pulmonary metastasis of 143B cells in orthotopic mouse osteosarcoma model. Expression microarrays are performed in143B-shCtrl and 143B-shIRX1 cells to study the mechanism of IRX1 on promoting metastasis of osteosarcoma
Project description:The goal of this study is to dig out DNA damage pathways mediated by VEGF-B. Using RNA-seq differential expression analysis, we observed genes involved in genomic stability maintainence were upregulated in VEGF-B treated HUVECs. Increased expression of 7 key DNA damage processing genes was confirmed by qRT–PCR. Our study displays the transcriptomic change of HUVECs in the early stage of VEGF-B treatment without strong stress and suggests that VEGF-B signal upregulates genes of DNA damage processing pathway in HUVECs.
Project description:The Hsp70 chaperone BiP is covalently modified with adenosine monophosphate (referred to as AMPylation) in order to adapt its activity to the fluctuating folding load within the endoplasmic reticulum. This modification is catalyzed by the only human representative of the family of filamentation induced by cyclic adenosine monophosphate (Fic) enzymes HYPE/FICD. The structural basis for BiP binding and AMPylation has remained elusive due to the low affinity of enzyme substrate complexes.
Project description:The prognosis of hepatocellular carcinoma (HCC) is poor due to the high incidence of intrahepatic metastasis. The aim of this study is to investigate the mechanism of intrahepatic metastasis in HCC via extracellular vesicles (EVs).
Project description:Pulmonary metastasis is the main cause of medical failure and death of osteosarcoma patients. Our recent study identified IRX1 as a potential metastasis-driving gene in osteosarcoma. Studies showed that IRX1 can promote the migration, invasion and anoikis resistance of osteosarcoma cells. We generated 143B stable IRX1 knockdown and control cell lines, and found that IRX1 knockdown can inhibit the pulmonary metastasis of 143B cells in orthotopic mouse osteosarcoma model.
2015-08-25 | GSE55958 | GEO
Project description:Public description (Provide a description of the study goals and relevance)
Project description:Mutations of the forkhead transcription factor FOXP2 gene have been implicated in inherited speech-and-language disorders, and specific Foxp2 expression patterns in neuronal populations and neuronal phenotypes arising from Foxp2 disruption have been described. However, molecular functions of FOXP2 are not completely understood. Here we report a requirement for FOXP2 in growth arrest of the osteosarcoma cell line 143B. We observed endogenous expression of this transcription factor both transiently in normally developing murine osteoblasts and constitutively in human SAOS-2 osteosarcoma cells blocked in early osteoblast development. Critically, we demonstrate that in 143B osteosarcoma cells with minimal endogenous expression, FOXP2 induced by growth arrest is required for up-regulation of p21WAF1/CIP1. Upon growth factor withdrawal, FOXP2 induction occurs rapidly and precedes p21WAF1/CIP1 activation. Additionally, FOXP2 expression could be induced by MAPK pathway inhibition in growth-arrested 143B cells, but not in traditional cell line models of osteoblast differentiation (MG-63, C2C12, MC3T3-E1). Our data are consistent with a model in which transient upregulation of Foxp2 in pre-osteoblast mesenchymal cells regulates a p21-dependent growth arrest checkpoint, which may have implications for normal mesenchymal and osteosarcoma biology.