Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA136283 | ENA |
REPOSITORIES: ENA
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Project description:Ribosomal protein RPL19 is an integral component of eukaryotic ribosomes and universally involved in protein synthesis. Although consistently stableM-BM- in normal cells, RPL19 transcription is relatively elevated in prostate cancer. Using siRNA, we inhibited RPL19 transcription and demonstrated the gene to be functionally involved in promoting the malignant phenotype. Reducing RPL19 modulates a subset of genes rather than globally down-regulating protein synthesis, as evidenced by Western blotting and maintenance of cell proliferation. Mechanistically, either all ribosomes are not structurally and functionally identical or absence of RPL19 is compensated by other ribosomal protein genes. Following RPL19 inhibition, gene expression analysis confirms induction of the non-malignant phenotype principally to involve perturbation of transcription factor networks and cellular adhesion genes. 10 microarray experiments were analysed using five different prostate cell types: PC3M, PNT2, PC3M with stable knockdown transfection, PC3M with a scrambled virus and various PC3M knockdowns pooled
2011-12-08 | E-GEOD-26774 | biostudies-arrayexpress
Project description:Ribosomal protein RPL19 is an integral component of eukaryotic ribosomes and universally involved in protein synthesis. Although consistently stable in normal cells, RPL19 transcription is relatively elevated in prostate cancer. Using siRNA, we inhibited RPL19 transcription and demonstrated the gene to be functionally involved in promoting the malignant phenotype. Reducing RPL19 modulates a subset of genes rather than globally down-regulating protein synthesis, as evidenced by Western blotting and maintenance of cell proliferation. Mechanistically, either all ribosomes are not structurally and functionally identical or absence of RPL19 is compensated by other ribosomal protein genes. Following RPL19 inhibition, gene expression analysis confirms induction of the non-malignant phenotype principally to involve perturbation of transcription factor networks and cellular adhesion genes.
2011-12-08 | GSE26774 | GEO
Project description:Knockdown of DHRS7 in the prostate cancer cell line LNCaP was performed for 24h, 36h, and 48h using siRNA.
2022-07-07 | PXD031229 | Pride
Project description:Aberrant expression of HOXC6 and HOXC4 is commonly detected in prostate cancer. The high expression of these transcription factors is associated with aggressive prostate cancer and can predict cancer recurrence after treatment. Thus, HOXC4 and HOXC6 are clinically relevant biomarkers of aggressive prostate cancer. However, the molecular mechanisms by which these HOXC genes contribute to prostate cancer is not yet understood. To begin to address the role of HOXC4 and HOXC6 in prostate cancer, we performed RNA-seq analyses before and after siRNA-mediated knockdown of HOXC4 and/or HOXC6 and also performed ChIP-seq to identify genomic binding sites for both of these transcription factors. Our studies demonstrate that HOXC4 and HOXC6 co-localize with HOXB13, FOXA1 and AR, three transcription factors previously shown to contribute to the development of prostate cancer. We suggest that the aberrantly upregulated HOXC4 and HOXC6 proteins may compete with HOXB13 for binding sites, thus altering the prostate transcriptome. This competition model may be applicable to many different human cancers that display increased expression of a HOX transcription factor.
2020-01-22 | GSE129951 | GEO
Project description:Effect of SUB1 knockdown on aggressive prostate cancer
| PRJNA301740 | ENA
Project description:Here we performed transcriptional profiling of the prostate cancer cell lines LNCaP and 22Rv1 comparing non-targeting siRNA treatment versus siRNAs targeting SWI/SNF complex proteins (SMARCA2, SMARCA4, and SMARCB1). Goal was to determine the effect of SWI/SNF knockdown on gene expression in prostate cancer. Two-condition experiment: non-targeting siRNA versus SWI/SNF-siRNA treated cells. Three SWI/SNF proteins were targeted: SMARCA2, SMARCA4, and SMARB1. Biological replicates: 1 control replicate, 2 treatment replicates per SWI/SNF protein. Technical replicates: 1 replicate per SWI/SNF protein. Cell lines: 22Rv1 and LNCaP.
2013-07-20 | E-GEOD-40384 | biostudies-arrayexpress
Project description:SChLAP1 is a novel long non-coding RNA expressed in prostate cancer. Here we performed transcriptional profiling of the prostate cancer cell lines LNCaP and 22Rv1 comparing non-targeting siRNA treatment versus SChLAP1-siRNA treatment. Goal was to determine the effect of SChLAP1 knockdown on gene expression in prostate cancer.
2013-07-20 | GSE40383 | GEO
Project description:Transcriptional profiling of LNCaP prostate cancer cells comparing control siRNA-treated LNCaP cells with LNCaP cells treated with siRNAs targeting Prostate Cancer Associated Transcript-1 (PCAT1), an uncharacterized long non-coding RNA. High-throughput sequencing of polyA+ RNA (RNA-Seq) in human cancer shows remarkable potential to identify both novel disease-specific markers for clinical uses and uncharacterized aspects of tumor biology, particularly non-coding RNA (ncRNA) species. To illustrate this approach, we employed RNA-Seq on a cohort of 102 prostate tissues and cells lines and found that aberrant expression profiles of novel tissue-specific ncRNAs distinguished benign, cancerous, and metastatic tumors. Among these, a novel prostate-cancer specific ncRNA (termed PCAT-1) defined a subset of aggressive cancers with low expression of the epigenetic regulator EZH2, a component of the Polycomb Repressive Complex 2 (PRC2) commonly upregulated in metastatic cancers. In vitro assays for core PRC2 genes indicated that the PRC2 complex directly binds and represses PCAT-1, and that the PCAT-1 transcript reciprocally binds PRC2, suggesting a regulatory feedback mechanism. Importantly, knockdown of PCAT-1 in cells with high levels of endogenous PCAT-1 transcript showed changes in cell proliferation and transcriptional regulation of several key biological processes, including cell cycle. Finally, we showed that ncRNA expression signatures, including PCAT-1, were effective for the non-invasive detection of prostate cancer, and that high ncRNA expression signature values correlate with high-grade histology. The findings presented herein establish the utility of RNA-Seq to comprehensively identify unannotated ncRNAs that define human disease states and characterize PCAT-1 as a novel regulator of cell proliferation mechanistically linked to PRC2 and contributory to translational clinical tests for prostate cancer. Two-condition experiment: Control-siRNA-treated versus PCAT1-siRNA-treated LNCaP cells. Biological replicates: 3 control replicates, 3 treatment replicates.
2011-07-27 | E-GEOD-29886 | biostudies-arrayexpress
Project description:Knockdown of the receptor tyrosine kinase EphB4 using siRNA in LNCaP prostate cancer cells compared to negative siRNA controls
2014-09-27 | GSE61800 | GEO
Project description:The transcription factor HOXC6 is upregulated in human prostate cancer. SiRNA knockdown of HOXC6 induces apoptosis in LNCaP cells while upregulation rescued LNCaP cells from siRNA-induced apoptosis. We used microarrays to identify the genes whose expression underly the anti-apoptotic and proliferative effects of HOXC6 in LNCaP cells. Keywords: transient overexpression and knockdown
2008-07-01 | GSE9182 | GEO