Project description:Human prostate cancer cells treated with shCSN5(sh37) or CSN5 inhibitior (CSN5i-3). Cells were treated with DMSO, 1uM (in C4-2), 5uM (in LNCaP, 22Rv1) or 10 uM (in PC3) CSN5i-3 for 48 hours. Cells were prepared for RNA-seq.
Project description:This study aimed to identify gene signatures induced by enzalutamide (ENZA) in hormone-sensitive (LNCaP) and hormone-resistant prostate cancer (PCa) cells. LNCaP and C4-2 cells were treated with ENZA alone or in combination with androgen deprivation therapy (ADT) and radiation (XRT). Through gene expression profiling, we identified that ENZA alone or in combination with ADT enhanced the effect the effect of XRT through immune-related pathways in LNCaP cells and metabolic pathways in C4-2 cells.Kaplan-Meier curve and Cox propotional hazard models showed that low expression of all the candidate genes except PTPRN2 were associated with tumor progression and recurrence in a PCa cohort.
Project description:LNCaP and its androgen insensitive derivative were profiled in order to identify genes differentially expressed during the conversion to androgen insensitivity. This experiment was performed due to the presence of an ins(7;14) localizing the entire ETV1 locus to chr 14 in LNCaP and C4-2B prostate cancer cells. Keywords: cell type comparison LNCaP and C4-2B were both hybridized to Agilent Whole Human Genome Oligonucleotide Microarrays, with a commercially obtained pool of benign prostate RNA serving as the reference for both cell lines. Dye flips for both cell lines were also performed
Project description:LNCaP prostate cancer cells were infected by lentivirus expressing either ctrl or HOTAIR, and the cells were cultured in hormone-deprived condition (Ethl) or in the presence of androgen (R1881). C4-2B prostate cancer cells were infected by lentivirus expressing either shCtrl or shHOTAIR, and the cells were cultured in hormone-deprived condition (Ethl) or in the presence of androgen (R1881).
Project description:Gene expression was first compared between control and NRP2 depletd condition in prostate adenocarcinoma cell line LNCaP C4-2B . In the next set, we compared the gene expression between control and AR deplted state in LNCaP C4-2B cells.
Project description:Castration resistant prostate cancer (CRPC) is a lethal disease. Sustained aberrant activation of androgen receptor (AR) becomes a central mechanism that contributes to endocrine therapy resistance. Here, we demonstrate that AR-bound enhancer RNAs (AR-eRNAs), including eRNA of the KLK3 (or PSA) gene, are upregulated in human CRPC cells and patient tissues. By enhancing C-termine domain (CTD) serine-2 phosphorylation of RNA polymerase II (Pol II-Ser2p), PSA eRNA acts in cis to promote PSA mRNA transcription and in trans to induce mRNA expression of a large set of genes involved in androgen action, cell cycle progression and tumorgenesis. Accordingly, we demonstrate that PSA eRNA binds in vitro and in vivo to CYCLIN T1, a regulatory subunit of the positive transcription elongation factor b (P-TEFb) complex that mediates Pol II-Ser2p. To identify the PSA eRNAâ??s functions on the Pol II-Ser2p and CYCLINT1 in the CRPC C4-2 cells, we detected the Pol II-Ser2p and CYCLINT1 ChIP-seq with or without PSA eRNA knockdown in the C4-2 cells. Moreover, to rule out the AR binding changes and identify the AR binding sites around the new genes, we detected the AR ChIP-seq in LNCaP and C4-2 cells with or without the androgen. Androgen receptor (AR) binding sites in human prostate cancer cell lines, LNCaP and C4-2, were studied using ChIP-seq. Pol II Ser-2p and CYCLINT1 binding sites in human prostate cancer cell lines C4-2 with or without PSA eRNA knockdown, were studied using ChIP-seq. ChIP enriched and input DNA were sequenced using Illumina HiSeq 2000.
Project description:NCOR2 is frequently and significantly mutated in late stage androgen deprivation therapy resistant prostate cancer (ADT-RPCa). NCOR2 has been characterized as a transcriptional corepressor and has mechanistic links to DNA methylation, but its global functions and overall contributions to PCa progression remain enigmatic. We mapped the dihydrotestosterone (DHT) dependent and independent effects of NCOR2 on the transcriptome, cistrome and DNA methylome in androgen sensitive (AS) and ADT-RPCa cells using the isogenic LNCaP and LNCaP-C4-2 (C4-2) cell models and the CWR22 xenograft model of ADT-RPCa.
Project description:LNCaP and its androgen insensitive derivative were profiled in order to identify genes differentially expressed during the conversion to androgen insensitivity. This experiment was performed due to the presence of an ins(7;14) localizing the entire ETV1 locus to chr 14 in LNCaP and C4-2B prostate cancer cells. Keywords: cell type comparison
