Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1036778 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:PiR-hsa-4447944 serves as an oncogenic mediator in prostate cancer and promotes the development of castration resistance by inhibiting NEFH expression
| PRJNA1041862 | ENA
Project description:PiR-hsa-4447944 showed a significantly higher expression level in both CRPC tissues and CRPC cell lines. Functionally, piR-hsa-4447944 overexpression conferred, whereas piR-hsa-4447944 suppression inhibited castration resistance ability in vitro and in vivo. Enforced piR-hsa-4447944 expression in vitro promoted PCa cells migration and invasion, as well as reduced cell apoptosis. To explore the potential targets of piR-hsa-4447944, two PCa cells 22RV1 and LNCaP were transfected with control or piR-hsa-4447944 mimic, and then the extracted total RNA was used for mRNA sequencing and bioinformatic analysis.
2024-07-17 | GSE248169 | GEO
Project description:Higher expression levels of DLX1 has been associated with primary and metastatic prostate tumor. DLX1 along with HOXC6 is well-established diagnostic biomarker for the early detection of prostate cancer (PCa). However, the mechanism involved in DLX1 up-regulation and functional significance in metastatic castration-resistant prostate cancer (mCRPC) progression remains unexplored. Here, we identified that DLX1 serves as an oncogene thereby regulating several oncogenic properties associated with PCa progression.
2021-07-30 | GSE138738 | GEO
Project description:Generally, only exonic circular RNA is believed to play the role as molecular sponge, while the main function of intronic circular RNA is regulating the expression of its parental gene. We aimed to find out whether intronic circular RNA could also act as molecular sponge in castration-resistance prostate cancer. Gene chip of castration-resistant and hormone-sensitive prostate cancer cell lines was sequenced to identify the differentially expressed circular RNA. We demonstrated that intronic circular RNA hsa_circ_0092339, located in the nucleus, was highly expressed in castration-resistance prostate cancer (CRPC) cell lines by using high throughput RNA sequencing. By knocking down hsa_circ_0092339, we found that this intronic circular RNA did not regulate the expression of its parental gene. By RIP and RNA pull-down experiment, we further found hsa_circ_0092339 realized its function by acting as molecular sponge. Hsa_circ_0092339 prevented degradation of C-MYC by absorbing hsa-mir-940 and preventing it enter the cytoplasm from nucleus. The combination of hsa-mir-940 and C-MYC was certified by dual-luciferase assay. In addition, we proved this axis was also effective in CRPC xenografted model. The effectiveness of this pathway in tissues was verified by animal experiments.
2023-01-01 | GSE185910 | GEO
Project description:Prostate tumor cells growth is interconected to androgen signaling. Indeed, the main line of treatment for advanced prostate cancer is focused on inhibiting androgen signaling by either surgical or pharmacological castration (or androgen-ablation, e.g. degarelix). We used microarrays to detail the global programme of gene expression following androgen-deprivation therapy (ADT) and identified distinct classes of up-regulated genes during this process that could contribute to the development of castration resistance.
2021-04-06 | GSE171491 | GEO
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.
2020-05-13 | PXD013340 | Pride
Project description:Acquisition of resistance to the PARP inhibitor, Olaparib, constitutes a major challenge for the treatment of advanced prostate cancer. The purpose of this study was to identify molecular targets responsible for the development of acquired Olaparib resistance in advanced prostate cancer. Towards this goal, next-generation sequencing (NGS)-based gene expression profiling (RNA-Sequencing; RNA-Seq) was performed on castration-sensitive prostate cancer (CSPC)/Olaparib-sensitive LNCaP cells, castration-sensitive prostate cancer (CSPC)/Olaparib-resistant LN-OlapR cells, castration-resistant prostate cancer (CSPC)/Olaparib-sensitive C4-2B cells, and castration-resistant prostate cancer (CSPC)/Olaparib-resistant 2B-OlapR cells.
2023-12-06 | GSE249514 | GEO
Project description:The androgen receptor (AR) is a mediator of both androgen-dependent and castration- resistant prostate cancers. Identification of cellular factors affecting AR transcriptional activity could in principle yield new targets that reduce AR activity and combat prostate cancer, yet a comprehensive analysis of the genes required for AR-dependent transcriptional activity has not been determined. Using an unbiased genetic approach that takes advantage of the evolutionary conservation of AR signaling, we have conducted a genome-wide RNAi screen in Drosophila cells for genes required for AR transcriptional activity and applied the results to human prostate cancer cells. We identified 45 AR-regulators, which include known pathway components and genes with functions not previously linked to AR regulation, such as HIPK2 (a protein kinase) and MED19 (a subunit of the Mediator complex). Depletion of HIPK2 and MED19 in human prostate cancer cells decreased AR target gene expression and, importantly, reduced the proliferation of androgen-dependent and castration-resistant prostate cancer cells. We also systematically analyzed additional Mediator subunits and uncovered a small subset of Mediator subunits that interpret AR signaling and affect AR-dependent transcription and prostate cancer cell proliferation. Importantly, targeting of HIPK2 by an FDA approved kinase inhibitor phenocopied the effect of depletion by RNAi and reduced the growth of AR-positive, but not AR negative, treatment-resistant prostate cancer cells. Thus, our screen has yielded new AR regulators including drugable targets that reduce the proliferation of castration-resistant prostate cancer cells. HIPK2 and MED19 were identified via a genome-wide RNAi screen as new androgen receptor (AR) reulators. Our goal in performing this microarray was to identify the gene regulated by HIPK2 and MED19 in a late stage prostate cancer cell line (LNCaP-abl), and to see what genes are in common with known genes to be regulated by AR, and what genes are unique to HIPK2 or MED19. Knockdown of HIPK2 and MED19 was tested in LNCaP-abl cells against control. Each was performed in duplicates. Six samples were analyzed
2013-01-30 | E-GEOD-43881 | biostudies-arrayexpress
Project description:Docetaxel-based chemotherapy is the standard first-line therapy in metastatic castration-resistant prostate cancer. However, most patients eventually develop resistance to this treatment. The aim of the study was to identify key molecular genes and networks associated with docetaxel resistance in 2 models of docetaxel-resistant castration-resistant prostate cancer cell lines.
2012-01-01 | GSE33455 | GEO
Project description:Androgen receptor (AR) is a hormone-activated transcription factor that plays important roles in prostate development, function, as well as malignant transformation. The downstream pathways of AR, however, are incompletely understood. AR has been primarily known as a transcriptional activator inducing prostate-specific gene expression. Through integrative analysis of genome-wide AR occupancy and androgen-regulated gene expression, here we report AR as a globally acting transcriptional repressor. This repression is mediated by androgen responsive elements (ARE) and dictated by Polycomb group protein EZH2 and repressive chromatin remodeling. In embryonic stem cells, AR-repressed genes are occupied by EZH2 and harbor bivalent H3K4me3 and H3K27me3 modifications that are characteristic of differentiation regulators, the silencing of which maintains the undifferentiated state. Concordantly, these genes are silenced in castration-resistant prostate cancer rendering a stem cell-like lack of differentiation and tumor progression. Collectively, our data reveal an unexpected role of AR as a transcriptional repressor inhibiting non-prostatic differentiation and, upon excessive signaling, resulting in cancerous de-differentiation. It provides an innovative mechanism for castration resistance and highlights novel therapeutic strategies to treat advanced prostate cancer. Keywords: Genetic Modification compare gene expression in different cell lines with or without androgen treatment or EZH2 knockdown
2011-12-11 | E-GEOD-31978 | biostudies-arrayexpress