MRNA expression profile in PCa And BPH from Chinese patients
Ontology highlight
ABSTRACT: To study the miRNA modulating network and different expressed miRNA lists in prostate cancer, we use hight-throught method to genomically detect the expression profile of miRNA, mRNA and protein. Agilent microarray products for miRNA and mRNA expression profile are choosed. As possible as we can to use the same sample for miRNA, mRNA and protein experiment. 4 prostate cancer and 4 normal tissue are applied to mRNA microarray experiment. The mRNA microaaray experiment service are supplied by ShanghaiBio Corporation(Shanghai,China).
Project description:To study the miRNA modulating network and different expressed miRNA lists in prostate cancer, we use hight-throught method to genomically detect the expression profile of miRNA, mRNA and protein.
Project description:To study the miRNA modulating network and different expressed miRNA lists in prostate cancer, we use high-throughout method to genomically detect the expression profile of miRNA, mRNA and protein. Agilent microarray products for miRNA and mRNA expression profile were chose. With GE Ettan DIGE System, the differentiated expression proteins are detected. As possible as we can to use the same sample for miRNA, mRNA and protein experiment. 4 prostate cancer tissues and 4 normal tissues are applied to mRNA microarray experiment. The mRNA microarray experiment service are supplied by ShanghaiBio Corporation (Shanghai,China).
Project description:To study the miRNA modulating network and different expressed miRNA lists in prostate cancer, we use high-throughout method to genomically detect the expression profile of miRNA, mRNA and protein.
Project description:This SuperSeries is composed of the following subset Series: GSE28204: mRNA expression profile in PCa And BPH from Chinese patients GSE34932: miRNA expression profile in PCa And BPH tissue from Chinese patients Refer to individual Series
Project description:MicroRNAs (miRNAs) play important roles in cell differentiation and self-renewal controlling post-transcriptional processing of mRNAs and attenuating production of the encoded proteins. Here, we unveil a novel oncogenic pathway leading to activation of STAT3 signaling through miRNA-mediated silencing of the E3 ubiquitin ligase COP1. miRNA profiling showed that miR-424 was upregulated in prostate cancer compared to normal prostate and specifically associated with reduced level of the ETS factor ESE3/EHF in an aggressive subgroup of tumors. MiR-424 was significantly elevated also in other epithelial cancers and amplified in 1-3% of various cancers. In normal prostate epithelial cells miR-424 was repressed by ESE3/EHF and when upregulated promoted oncogenic and cancer stem cell (CSC) properties. Conversely, ablation of miR-424 in metastatic prostate cancer cells reduced CSC self-renewal and prevented in vivo tumour initiation and metastatic spread. miR-424 targeted the 3' UTR of COP1 mRNA and reduced COP1 protein level. COP1 induced STAT3 ubiquitylation and degradation by the ubiquitin-proteasome system (UPS). Therefore, reduced levels of COP1 in prostate cancer cells, resulted in accumulation and increased STAT3 signaling. COP1 knockdown and over-expression phenocopied the effects of miR-424 deregulation on oncogenic phenotypes and STAT3 signalling, while STAT3 knockdown prevented the transforming effects of miR-424. Consistently, expression of EHF/ESE3 and RFWD2/COP1 were highly correlated in human prostate cancers and other epithelial tumors. Furthermore, miR-424 induced genes were enriched of STAT3 targets, converged with those induced by COP1 loss in mouse embryos and were associated with adverse prognosis in prostate and other epithelial cancers. In primary prostate tumours, low COP1 and high STAT3 protein level were also significantly associated and predictive of biochemical relapse. Collectively, this study reveals a novel miRNA-activated oncogenic axis in prostate cancer. Targeting miR-424 or miR-424 dependent pathways may represent a unique approach to attack a key node in tumorigenesis.
Project description:Prostate cancer is the most commonly diagnosed oncogenic malignancy in men worldwide, resulting in almost 30,000 cancer-related deaths in the United States each year. Wider examination of aberrant glycosylation in prostate cancer has revealed increased expression of the glycotransferase involved in core fucosylation, (1,6)fucosyltranferase (FUT8) associating with aggressive (AG) prostate cancer and castration-resistance, with functional analyses revealing FUT8 impacting cell motility and invasiveness in prostate cancer cells. Exosomes are extracellular microvesicles (30-150 nm) that are involved in in both proximal and distal intercellular communication via the transport of proteins and nucleic acids (mRNA, miRNA, and DNA). To gain insight into the impact of increased cellular FUT8 expression on exosome biogenesis and protein cargo profiles in prostate cancer, we paired Nanoparticle Tracking Analysis (NTA) and stable isotope labelling with amino acids in cell culture (SILAC) quantitative proteomics.
Project description:Copy number variations (CNVs) in the human genome have been linked to various carcinomas including prostate cancer (PCa). This study was conducted to identify CNVs in high grade PCa. We performed a pilot genome-wide CNV analysis in 36 subjects (18 high grade PCa and 18 benign prostatic hyperplasia) using array comparative genomic hybridization (aCGH) technique. Array results were validated using PCR-based copy number counting method. A total of 339 CNV regions were found to be unique to PCa subjects in this cohort (P < 0.05). Data segregation and filtering revealed six putative CNV loci associated with susceptibility to PCa. Of these, four were rare (1q21.3, 15q15, 3q27.2 and 7p12.1) and one was a novel copy number gain (12q23.1), harbouring genes such as the ARNT, THBS1, SLC5A8 and DDC which are crucial in the p53 and cancer pathways. Another CNV was a loss at 8p11.21 which contains the SFRP1 gene from the Wnt signalling pathway, known for its interaction with androgen receptors as reported for urological malignancy. Cross comparison analysis with genes already known to be associated with PCa revealed significant CNVs involved in crucial biological processes that elicit cancer pathogenesis via cytokine production, disease progression through endothelial cell proliferation and xenobiotic metabolism. In conclusion, these findings suggest that the CNV regions identified could provide an insight into the development of high grade PCa.
Project description:For androgen-independent prostate cancer (AIPC), the current treatment is limited and the prognosis is poor. We previously found miR-200b could inhibit androgen independent proliferation ability of prostate cancer cells, but the mechanism is unclear. MiRNAs plays their role by blocking translation through base-pairing with complementary mRNA and by promoting degradation of target mRNA. Unraveling the miRNA translational silencing network remains a challenge in part because a single miRNA can inhibit multiple mRNA targets and because a single mRNA can be regulated by several distinct miRNAs that act cooperatively. However, proteomics methods provide us useful tools to unravel the target genes network. This study identified the target genes of miR-200b in AIPC. It helps us to understand the mechanism of AIPC and applies several new candidate targets of AIPC treatment.