Project description:Histone deacetylase (HDAC) inibitors suppress cell proliferation of prostate cancer, but the detailed mechanisms are unknown. Moreover, HDAC includes 18 family members, namely HDAC1-11 and SIRT1-7, and differences of effects on prostate cancer proliferation among these enzymes are also unknown. Thus, we clarified differences of gene expression between prostate cancer cell line (LNCaP) treated with pan-HDAC inhibitors (TSA and OBP-801) or selective HDAC inhibitor (NCC-149, HDAC8-specific inhibitor)using cDNA microarray. LNCaP treated with TSA (1μM), NCC149 (2μM), OBP-801 (200nM) or DMSO for 24hrs, RNA was extracted from cells, and cDNA array was performed.
Project description:We optimized ChIP-sequencing protocole and anti-androgen receptor (AR) antibodies on human prostate cancer cell line (LNCaP) after either DMSO (solvent) or DHT 100nM 4 hours treatment.
Project description:N-butylidenephthalide (BP) exhibits its antitumor effect in a variety of cancer cell lines. However, little is known about its effects on prostate cancer. The objective of this study was to obtain additional insights into the mechanisms involved in BP induced cell death in human prostate cancer cells. To determine the mechanisms of BP-induced growth arrest and cell death in prostate cancer cell lines, we performed a microarray study to identify alterations in gene expression induced by treatment with BP in the LNCaP cells. LNCaP cellss were selected to treated with BP for 3 or 24hr for RNA extraction and hybridization on Affymetrix microarrays.
Project description:Prostate cancer is the most common cancer in men and AR downstream signalings promote prostate cancer cell proliferation. Although initially hormone-deprovation therapy is effective to inhibit cancer progression, most of cancers relapse as castration-resistant prostate cancer (CRPC). PSF is one of RNA binding proteins associated with prostate cancer progression. In this study, we examined the effect of small molecule treatment interacting with PSF in CRPC cells. In order to investigate the effect of small molecule interacting with PSF cells, we analyzed gene expression profile in AR-positive prostate cancer cell line LNCaP and CRPC model cell derived from LNCaP cells.We treated LNCaP cells with vehicle or dihydrotestosterone (DHT) for 24 h. LTAD cells were treated with siControl or siPSF (10 nM) for 48 h. LTAD cells were treated with vehicle or small molecule interacting with PSF (No.10-3) for 48 h.
Project description:Transcriptional profiling of human prostate cancer cell line LNCaP treated with Metformin or AICAR compared to control non-stimulated LNCaP.
Project description:Genome-wide DNA methylation profiling of human PC3 invasive prostate cancer cell line treated with vehicle control (SAH, S-adenosylhomocysteine) and with SAM (S-adenosylmethionine) as well as of untreated human LNCaP non-invasive prostate cancer cell line. The Illumina Infinium 450k Human DNA Methylation BeadChip v1.2 was used to obtain DNA methylation profiles across approximately 450,000 CpGs in human cell lines exposed to described treatments. Samples included biological triplicate of PC3 control (SAH treated), biological triplicate of PC3 treated with SAM, and biological duplicate of LNCaP untreated.
Project description:Methylation profiling of human prostate cancer tissues and cell lines. We mapped the global DNA methylation patterns in prostate tissues (n=17) and cells (n=2) from fifty nanograms of genomic DNA using Methylplex-Next Generation Sequencing (M-NGS). In addition, genes methylated in LNCaP and significantly overexpressed after 5’Azacytidine treatment of LNCaP cells are assessed by Agilent gene expression microarray. The comprehensive methylome map presented here will further our understanding of epigenetic regulation of the prostate cancer genome. [Gene expression] Two-condition experiment, control DMSO-treated vs. 5'aza-treated LNCaP at two time points (@24 and 48 hours) in replicates.
Project description:High levels of GLI (GLI1 and GLI2) mRNA and GLI luciferase reporter activity were detected in the androgen independent prostate cancer cell lines DU145 and PC-3 compared to the androgen-dependent LNCaP prostate cancer cell line. Subsequently, we observed that ectopic GLI1 promoted hormone independence in LNCaP cells (LNCaP-GLI1). We compared the gene expression profile of LNCaP-pBP (empty vector), LNCaP-GLI1, DU145, and PC-3 cells globally as well as to identify GLI1-regulated genes that may contribute to hormone independence.
