Project description:Project Description: Extracellular vesicles were isolated from conditioned media of prostate cancer cell lines PC-3M and LNCaP. Proteomic profiling was conducted on EVs to identify differential protein cargoes.
Project description:BACKGROUND. Human prostate cancer LNCaP and PC-3 cell lines have been extensively used as prostate cancer cell models to study prostate cancer progression and to develop therapeutic agents. Although LNCaP and PC-3 cells are generally assumed to represent early and late stages of prostate cancer development, respectively, there is limited information regarding comprehensive gene expression patterns between these two cells lines and relating these cells to prostate cancer progression based on their gene expression. METHODS. Comprehensive gene expression analysis was performed in LNCaP and PC-3 cells. Total RNA was isolated from cultured cells and hybridized to Illumina human Ref-8 version 3 BeadChips representing 24,526 transcripts. Bioinformatics approach was applied to identify genes, their functional roles and interaction networks that are unique in either LNCaP or PC-3 cells. RESULTS. We observed large differences in gene expression between LNCaP and PC-3 cells.Using robust statistical analysis and very high significance criteria to identify tractable number of genes 115 and 188 genes were identified uniquely expressed in LNCaP and PC-3 cells, respectively. Genes uniquely expressed in LNCaP cells contained UDP-glucosyltransferases as a signature for this cell line. This cell line demonstrated upregulation of various metabolic pathways on gene expression level. Talα/β, GATA-1 and c-Myc/Max were identified by in silico analysis as possible transcription factors regulating unique LNCaP genes. PC-3 cells were characterized by cytosceleton-related genes, keratins in particular. Several other well known genes (VEGFC, IL8, TGFβ2 and others) scattered throughout literature were identified and summarized in the discussion. CONCLUSIONS. This study demonstrated that LNCaP and PC-3 cells represent two distinct prostate cancer cell lineages. LNCaP cells retain many prostate cell specific properties, whereas PC-3 cells have acquired more aggressive bone-like characteristics following bone metastasis and show little resemblance to prostate cells. Microarray studies confirmed previously published results and provided more information between these two prostate cancer cell lines. Future studies need to consider their similarities and differences in gene expression between localized and metastasized prostate cancer.
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. RNA was harvested and analysed from LNCap-pBP (control/reference sample), LNCaP-GLI1, DU145 and PC-3 cells
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.
Project description:We measured the effect of docetaxel treatment to three differentially responsive prostate cancer cell lines, LNCaP, DU145 and PC-3, based on a transcriptional time course response by microarray analysis. These cell lines represent both androgen independent (DU145 and PC-3) and androgen sensitive (LNCaP) cells
Project description:Gene expression of 5 prostate cancer cell lines (LNCaP, VCaP, DU-145, PC-3, DuCaP) in standard culture conditions, harvested during exponential growth phase.
Project description:Microarray-based DNA methylation and gene expression profiling was carried out using a panel of prostate cancer cell lines (LNCaP-FGC, DU-145, and PC-3) and the control normal prostate RWPE1 cell line. The identification of prostate cancer-specific methylation markers was based on the following criteria: a difference in DNA methylation level (β) of at least 0.5, and at least a 2-fold difference in expression level between cancer and control cells. Using highly stringent selection criteria, we identified novel hypermethylated genes whose expression was silenced in prostate cancer cells.
Project description:The aberrant activation of HER2 has a pivotal role in bone metastasis implantation and progression in several tumor types, in-cluding prostate cancer (PC). Trastuzumab and other anti-HER2 therapies, such as lapatinib, have been used in human breast cancer HER2 positive. Although HER2 overexpression has been reported in PC, anti-HER2 therapy response has revealed conflicting results. We investigated the potential of lapatinib in inhibiting cell migration and inducing apoptosis in two human (LNCaP and PC3) and two canine PC cell lines (PC1 and PC2). Cell migration and apoptosis were evaluated by Annexin V/PI analysis after lapatinib treatment. The transcriptome analysis of all cell lines before and after treatment with lapatinib was also performed. We found increased apoptosis and migration inhibition in LNCaP cells (androgen-sensitive cell line), while PC1, PC2, and PC3 cells showed no alterations after the treatment. The transcriptome analysis of LNCaP and PC3 cell lines showed 158 dysregulated transcripts in common, while PC1 and PC2 cell lines presented 82. At the doses of lapatinib used, we observed transcriptional modifications in all cell lines. PI3K/AKT/mTOR pathway were enriched in human PC cells, while canine PC cells showed en-richment of tyrosine kinase antitumor response and HER2-related pathways. In canine PC cells, the apoptosis failed after lapatinib treatment, possibly due to the downregulation of MAPK genes. Prostate cancer cells insensitive to androgens may be resistant to lapatinib through PI3K gene dysregulation. The association of lapatinib with PI3K inhibitors may provide a more effective anti-tumor response and clinical benefits to PC patients.