Project description:Expression profiling of isoflavone and 3,3’-diindolylmethane treated C4-2B prostate cancer cells was conducted using Affymetrix Human Genome U133 Plus 2.0. Array C4-2B prostate cancer cells were treated with isoflavone and B-DIM for 6 hours or longer up to 72 hours. Gene expression profiling was conducted
Project description:Expression profiling of isoflavone and 3,3’-diindolylmethane treated C4-2B prostate cancer cells was conducted using Affymetrix Human Genome U133 Plus 2.0. Array
Project description:Identifying the effect of the co-chaperone SGTA on global androgen receptor transcriptional activity in C4-2B prostate cancer cells with view to further elucidating the broader biological role of SGTA on other signaling pathways within prostate cancer cells Knockdown of SGTA for 72 hours in C4-2B cells significantly altered the expression of approximately 1900 genes in both vehicle and DHT treated cells. The effect of SGTA knockdown was to suppress the expression of approximately 60% of those transcripts. The regulation of 35% of DHT target genes was also affected by SGTA knockdown, with gene-specific effects on basal, or DHT-induced expression, or both.
Project description:Identifying the effect of the co-chaperone SGTA on global androgen receptor transcriptional activity in C4-2B prostate cancer cells with view to further elucidating the broader biological role of SGTA on other signaling pathways within prostate cancer cells Knockdown of SGTA for 72 hours in C4-2B cells significantly altered the expression of approximately 1900 genes in both vehicle and DHT treated cells. The effect of SGTA knockdown was to suppress the expression of approximately 60% of those transcripts. The regulation of 35% of DHT target genes was also affected by SGTA knockdown, with gene-specific effects on basal, or DHT-induced expression, or both. C4-2B cells were transfected with 5nM non-specific control siRNA (NS) or with a pool of three commercially avaliable SGTA specific siRNA (SGTA) for 72hrs. Cells were subsequently treated with either ethanol vehicle control or 1nM DHT for 16hr. Total RNA was extracted. Five independent vehicle and 2 DHT siNS and siSGTA samples were hybridized to Affymetrix Human Gene 1.0 ST array chips.
Project description:Prostate cancer C4-2B cells were cultured in enzalutamide in a dose-escalation manner. After sixty passages cells were resistant to enzalutamide, with a specific sets of genes been deregulated. We performed global gene expression analysis by cDNA microarrays to identify genes responsible for enzalutamide resistance in C4-2B-MDVR cells. Enzalutamide resistant C4-2B-MDVR cells were selected from C4-2B cells during long time enzalutamide treatment. Genes responsible for enzalutamide resistance were identified using C4-2B vs. C4-2B-MDVR RNA extraction and hybridization on Affymetrix microarrays.
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.
Project description:Prostate cancer C4-2B cells were cultured in enzalutamide in a dose-escalation manner. After sixty passages cells were resistant to enzalutamide, with a specific sets of genes been deregulated. We performed global gene expression analysis by cDNA microarrays to identify genes responsible for enzalutamide resistance in C4-2B-MDVR cells.
Project description:Prostate cancer C4-2B cells were cultured in docetaxel in a dose-escalation manner. After nine months selection, cells were able to divide freely in 5 nM docetaxel, with a specific sets of genes been deregulated. We performed global gene expression analysis by cDNA microarrays to identify genes responsible for docetaxel resistance in TaxR cells. Docetaxel resistant TaxR cells were selected from C4-2B cells during long time docetaxel treatment. Genes responsible for docetaxel resistance were identified using C4-2B vs. TaxR RNA extraction and hybridization on Affymetrix microarrays.
Project description:Clinically, osteolytic phenotype is rare in prostate cancer. The molecular mechanism of bone metastasis in PCa is not fully understood. We performed RNA-seq to identify osteogenic and tumor associated roles in prostate cancer by a co-culture of osteoblasts (MG63) and prostate cancer cells (C4-2, C4-2B, 22Rv1 and DU145). We compared osteoblastic prostate cancer with osteolytic prostate cancer to evaluate the difference in phenotype of bone metastasis.