RNAseq analysis of prostate cancer stem cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE134428 | GEO | 2020/04/13
REPOSITORIES: GEO
Similar Datasets
Project description:Prostate cancer cells (PC3) were treated with purified human recombinant CRISP3 protein or vehicle control for 4 hours before whole cell protein extraction
2020-07-15 | PXD009609 | JPOST Repository
Project description:To uncover the mechanism underlying the effect of pentamidine on prostate cancer cells, we performed RNA sequencing (RNA-seq) to compare the transcriptional difference between pentamidine- and vehicle-treated prostate cancer cells (PC3 and DU145 cells).
2019-06-14 | GSE132693 | GEO
Project description:BACKGROUND: Cancer stem-like cells are proposed to sustain solid tumors by virtue of their capacity for self-renewal and differentiation to cells that comprise the bulk of the tumor, and have been identified for a variety of cancers based on characteristic clonal morphologies and patterns of marker gene expression. METHODS: Single cell cloning and spheroid culture studies were used to identify a population of cancer stem-like cells in the androgen-independent human prostate cancer cell line PC3. RESULTS: We demonstrate that, under standard culture conditions, ~10% of PC3 cells form holoclones with cancer stem cell characteristics. These holoclones display high self-renewal capability in spheroid formation assays under low attachment and serum-free culture conditions, retain their holoclone morphology when passaged at high cell density, exhibit moderate drug resistance, and show high tumorigenicity in scid immunodeficient mice. PC3 holoclones readily form spheres, and PC3-derived spheres yield a high percentage of holoclones, further supporting their cancer stem cell-like nature. We identified one gene, FAM65B, whose expression is consistently up regulated in PC3 holoclones compared to paraclones, the major cell morphology in the parental PC3 cell population, and two genes, MFI2 and LEF1, that are consistently down regulated. This molecular profile, FAM65Bhigh/MFI2low/LEF1low, also characterizes spheres generated from parental PC3 cells. The PC3 holoclones did not show significant enriched expression of the putative prostate cancer stem cell markers CD44 and integrin α2β1. PC3 tumors seeded with holoclones showed dramatic down regulation of FAM65B and dramatic up regulation of MFI2 and LEF1, and unexpectedly, a marked increase in tumor vascularity compared to parental PC3 tumors, suggesting a role of cancer stem cells in tumor angiogenesis. CONCLUSIONS: These findings support the proposal that PC3 tumors are sustained by a small number of tumor-initiating cells with stem-like characteristics, including strong self-renewal and pro-angiogenic capability and marked by the expression pattern FAM65Bhigh/MFI2low/LEF1low. These markers may serve as targets for therapies designed to eliminate cancer stem cell populations associated with aggressive, androgen-independent prostate tumors such as PC3. (Mol Cancer. 2010 Dec 29;9:319. doi: 10.1186/1476-4598-9-319; PMID: 21190562; PMCID: PMC3024252).
2013-11-07 | GSE52161 | GEO
Project description:Validation, by mass spectrometry (MS), of predicted neoantigens in urinary extracellular vesicles coming from cancer prostate patients. We performed MS on PC3, LNCaP and HCT116 cells and compared MS-detected peptides with established PC3 lncRNA peptides, peptides from lncRNAs upregulated in uEVs and Swiss prot databanks.
2022-05-31 | PXD032264 | Pride
Project description:Dynamic interaction between prostate cancer and the bone microenvironment is a major contributor to metastasis of prostate cancer to bone. In this study we utilized an in-vitro co-culture model of PC3 prostate cancer cells and osteoblasts followed by microarray based gene expression profiling to identify previously unrecognized prostate cancer-bone microenvironment interactions. Factors secreted by PC3 cells resulted in the up-regulation of many genes in osteoblasts associated with bone metabolism and cancer metastasis, including Mmp13, Il-6 and Tgfb2, and down-regulation of Wnt inhibitor Sost. To determine whether altered Sost expression in the bone microenvironment has an effect on prostate cancer metastasis, we co-cultured PC3 cells with Sost knockout (SostKO) osteoblasts and wildtype (WT) osteoblasts and identified several genes differentially regulated between PC3-SostKO osteoblast co-cultures and PC3-WT osteoblast co-cultures. Co-culturing PC3 cells with WT osteoblasts up-regulated cancer-associated long noncoding RNA (lncRNA) MALAT1 in PC3 cells. MALAT1 expression was further enhanced when PC3 cells were co-cultured with SostKO osteoblasts and treatment with recombinant Sost down-regulated MALAT1 expression in these cells. Our results suggest that reduced Sost expression in the tumor microenvironment may promote bone metastasis by up-regulating MALAT1 in prostate cancer.
2015-09-30 | GSE73044 | GEO
Project description:BACKGROUND: Cancer stem-like cells are proposed to sustain solid tumors by virtue of their capacity for self-renewal and differentiation to cells that comprise the bulk of the tumor, and have been identified for a variety of cancers based on characteristic clonal morphologies and patterns of marker gene expression. METHODS: Single cell cloning and spheroid culture studies were used to identify a population of cancer stem-like cells in the androgen-independent human prostate cancer cell line PC3. RESULTS: We demonstrate that, under standard culture conditions, ~10% of PC3 cells form holoclones with cancer stem cell characteristics. These holoclones display high self-renewal capability in spheroid formation assays under low attachment and serum-free culture conditions, retain their holoclone morphology when passaged at high cell density, exhibit moderate drug resistance, and show high tumorigenicity in scid immunodeficient mice. PC3 holoclones readily form spheres, and PC3-derived spheres yield a high percentage of holoclones, further supporting their cancer stem cell-like nature. We identified one gene, FAM65B, whose expression is consistently up regulated in PC3 holoclones compared to paraclones, the major cell morphology in the parental PC3 cell population, and two genes, MFI2 and LEF1, that are consistently down regulated. This molecular profile, FAM65Bhigh/MFI2low/LEF1low, also characterizes spheres generated from parental PC3 cells. The PC3 holoclones did not show significant enriched expression of the putative prostate cancer stem cell markers CD44 and integrin M-NM-12M-NM-21. PC3 tumors seeded with holoclones showed dramatic down regulation of FAM65B and dramatic up regulation of MFI2 and LEF1, and unexpectedly, a marked increase in tumor vascularity compared to parental PC3 tumors, suggesting a role of cancer stem cells in tumor angiogenesis. CONCLUSIONS: These findings support the proposal that PC3 tumors are sustained by a small number of tumor-initiating cells with stem-like characteristics, including strong self-renewal and pro-angiogenic capability and marked by the expression pattern FAM65Bhigh/MFI2low/LEF1low. These markers may serve as targets for therapies designed to eliminate cancer stem cell populations associated with aggressive, androgen-independent prostate tumors such as PC3. (Mol Cancer. 2010 Dec 29;9:319. doi: 10.1186/1476-4598-9-319; PMID: 21190562; PMCID: PMC3024252). Four PC3 cell-derived holoclones, selected based on their clear and unambiguous holoclone morphology and designated holoclones 2H10, 2G7, 1A8 and 5A2, were used for global transcriptome/microarray analysis in direct comparison to parental PC3 cells. Total RNA was prepared from each of four sequential cell passages for each PC3-derived holoclone, and from four passages of parental PC3 cells, 48 h after seeding the cells at 100,000 cells per well of a 6-well plate. For each sample (holoclones or parental PC3 cells), a pool of RNA was prepared by combining equal amounts of RNA from each passage to minimize the effects of passage number and inter-sample variability on gene expression profiles. All RNAs had an RNA integrity number >8.0, determined using an Agilent Bioanalyzer 2100 instrument. cDNAs transcribed from pools of RNA for each holoclone, and for parental PC3 cells, were labeled with Alexa 647 or Alexa 555 dyes in a fluorescent reverse pair (dye swap) design for competitive hybridization to Agilent Whole Human Genome Microarrays.
2013-11-07 | E-GEOD-52161 | biostudies-arrayexpress
Project description:Exosomes are an emerging source for biomarkers in various diseases. Prostate cancer is the most frequent cancer in men in industrialized countries. The only biomarker widely used is prostate specific antigen with its clinical relevance suffering from low specificity. To identify novel biomarker candidates for prostate cancer we isolated exosomes from the supernatant of malignant PC3 and benign PNT1A cells, grown under standard culture conditions, using sequential centrifugation and ultracentrifugation. Not to alter the cellular growth conditions an FBS-containing medium was used. As control this medium was also subjected to exosomen isolation. Exosome and control samples were analyzed on an LTQ-Orbitrap XL mass spectrometer and subsequently between 441 and 843 proteins per sample were identified by searching against the SwissProt database. 64 proteins exclusively found in PC3 exosomes were subjected to a scoring system, integrating data from five publicly accessible databases and literature search, to identify potential biomarker candidates. Among these the epithelial tight junction protein claudin-3 achieved the highest score. Retests under serum-free conditions using immunoblotting and immunogold-labeling confirmed the expression of claudin-3 on PC3 exosomes. Levels of circulating claudin-3 directly determined from blood plasma, without prior isolation of exosomes, using ELISA were significantly higher (p=0,038) in metastatic prostate cancer patients (n=15) compared to controls with histologically proven benign prostate hyperplasia (n=15). Our results for the first time describe claudin-3 as a potential biomarker candidate in prostate cancer, easily detectably using liquid biopsies, without need for laborious isolation of exosomes. Further studies including larger patient cohorts in different clinical states of prostate cancer are needed to validate our findings.
2017-04-13 | PXD003651 | Pride
Project description:We previously found that KLF4, a gene highly expressed in adult prostate stem cells, blocks the progression of indolent intraepithelial prostatic lesions into aggressive and rapidly growing tumors. To test whether this anti-cancer effect of KLF4 can also prevent prostate cancer-induced damage to the bone, we ablated KLF4 in human PC3 prostate cancer cells using CRISPR/Cas9-mediated genome editing and compared their behavior to null cells transduced with a DOX inducible KLF4 expression system. KLF4 re-expression inhibited growth of PC3 null cells in monolayer and as colonies in soft agar in a dose-dependent manner. When injected into the mouse femurs, PC3 null cells proliferated rapidly, forming very large, invasive and osteolytic tumors. Induction of KLF4 expression in PC3 null cells immediately after their intra-femoral inoculation blocked the development of tumors while preserving the normal bone architecture. KLF4 re-expression in established PC3 bone tumors inhibited osteolytic effects of PC3 null cells, preventing bone fractures and inducing a significant osteogenic response with regions of new bone formation. Transcriptome analyses of PC3 cells with no or high KLF4 expression revealed KLF4-dependent osteolytic or osteogenic transcriptional programs, respectively. Importantly, these KLF4-dependent functions significantly overlapped with metastatic prostate cancers in patients.
2019-05-09 | GSE117965 | GEO
Project description:RNAseq analysis of prostate cancer stem cells
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Project description:To investigate the role of PDEF in prostate cancer metastasis, we employed microarray analysis of PC3 cells ectopically expressing a pBABE vector control (PC3-SCR) or PDEF-containing vector (PC3-PDEF).
2020-01-24 | GSE108641 | GEO