Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA168493 | ENA |
REPOSITORIES: ENA
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Project description:Disseminated prostate cancer cells colonize the skeleton to progress into macroscopic lesions only if they successfully adapt to the bone microenvironment. We previously reported that the ability of prostate cancer cells to generate skeletal tumors in animal models correlated with the expression of the alpha-receptor for Platelet-Derived Growth Factor (PDGFRa). In this study we aimed to identify PDGFRa-regulated genes responsible for the acquisition of a bone-metastatic prostate phenotype. We performed genome-wide expression comparative analyses of human prostate cancer cell lines that differ for PDGFRa expression and propensity to establish tumors in the skeleton of animal models. We investigated the genes that were differentially regulated in the highly bone-metastatic PC3-ML cells and their low-metastatic counterpart PC3-N cells, and the genes differentially regulated between PC3-N and PC3-N with overexpression of PDGFRa (PC3NRa). We have previously shown that DU-145 cells lack PDGFRa and fail to survive longer than three days as disseminated tumor cells after homing to the mouse bone marrow. Interestingly, and in contrast to PC3-N cells, the exogenous expression of PDGFRa did not promote metastatic bone-tropism of DU-145 cells in our model. Thus, we examined the genes that were differentially regulated between DU-145 and DU-145(Ra) and excluded them from our candidate genes. Finally, to refine our findings and compensate for PC3 and DU-145 genetic disparity, we performed a comparative analysis of the genes differentially regulated between two bone metastatic single-cell progenies that were derived from PC3-ML cells. Seven human prostate cancer cell lines were analyzed in total for this study. Each cell line was analyzed in duplicate from two different passages in culture.
2013-03-30 | E-GEOD-43332 | biostudies-arrayexpress
Project description:Disseminated prostate cancer cells colonize the skeleton to progress into macroscopic lesions only if they successfully adapt to the bone microenvironment. We previously reported that the ability of prostate cancer cells to generate skeletal tumors in animal models correlated with the expression of the alpha-receptor for Platelet-Derived Growth Factor (PDGFRa). In this study we aimed to identify PDGFRa-regulated genes responsible for the acquisition of a bone-metastatic prostate phenotype. We performed genome-wide expression comparative analyses of human prostate cancer cell lines that differ for PDGFRa expression and propensity to establish tumors in the skeleton of animal models. We investigated the genes that were differentially regulated in the highly bone-metastatic PC3-ML cells and their low-metastatic counterpart PC3-N cells, and the genes differentially regulated between PC3-N and PC3-N with overexpression of PDGFRa (PC3NRa). We have previously shown that DU-145 cells lack PDGFRa and fail to survive longer than three days as disseminated tumor cells after homing to the mouse bone marrow. Interestingly, and in contrast to PC3-N cells, the exogenous expression of PDGFRa did not promote metastatic bone-tropism of DU-145 cells in our model. Thus, we examined the genes that were differentially regulated between DU-145 and DU-145(Ra) and excluded them from our candidate genes. Finally, to refine our findings and compensate for PC3 and DU-145 genetic disparity, we performed a comparative analysis of the genes differentially regulated between two bone metastatic single-cell progenies that were derived from PC3-ML cells.
2013-03-30 | GSE43332 | GEO
Project description:We describe the gene expression profile of metastasis-prone lungs of mice after injection of LN4-tumor cell conditioned media intraperitoneally for one week, compared to the metastasis-inhibitory PC3 tumor cell conditioned media, which is the parental cell line to LN4 2 mice injected with RPMI medium (control), 2 mice injected with PC3-derived conditioned medium, and 2 mice injected with PC3M-LN4 conditioned medium
2014-02-01 | E-GEOD-44459 | biostudies-arrayexpress
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:PC3 are a metastatic prostate cancer cell line. Microarray analysis was performed to evaluate the impact of miR-149-3p overexpression or DAB2IP depletion in PC3.
2018-10-01 | GSE104353 | GEO
Project description:We overexpressed the long non-coding RNA GHSROS in the metastatic prostate cancer cell line PC3.
2019-11-14 | GSE86097 | GEO
Project description:To elucidate the regulation of NSD2 in metastatic castration-resistant prostate cancer(CRPC), we performed Hi-C against castration-sensitive prostate cancer cell line LNCaP and metastatic castration-resistant prostate cancer cell lines, PC3 respectively. In metastatic CRPC, we found specific regions of activation with epigenetic changes.
2024-09-04 | GSE248627 | GEO
Project description:Prostate cancer (PCa) is the most common cancer in American men. The American Cancer Society’s estimates for prostate cancer in the United States for 2017 are estimated 161.360 new cases and 26,730 deaths from PCa. To study metastatic properties to bone, PC-3 cell line is mainly used classical human prostatic carcinoma cell line, established and characterized its tumorigenicity from a human prostatic adenocarcinoma metastatic to bone is reported. In addition, PC-3/nkR cell line, natural killer(NK) cells-resistant, was isolated from mammary tumor xenograft studies in mice from PC-3 was implanted to nude mice and fecund to be tumorigenic in the early 2000s. In this study, we investigated secreted proteins of the conditioned media of PC-3 and PC-3/nkR cell lines using comparative proteomics technology to identify the molecular mechanism related to metastatic processes related to PC-3/nkR. Our study showed PC-3/nkR cells are new highly migrated and NK cells-resistant cell-line compared to PC-3 cells, as novel highly malignant tumor cells to study mechanisms of PCa metastatic.
2019-08-19 | PXD008184 | Pride
Project description:Our goal was to determine whether osteoblastic LuCaP 23.1 prostate cancer xenograft tumors can elicit an osteoblastic response at the gene expression level in human bone marrow stromal cells. Custom Agilent 44K whole human genome expression oligonucleotide microarrays were used to profile bone marrow stroma cells isolated from three patients and treated with either mineralization media or LuCaP 23.1 conditioned medium. Total RNA was isolated and amplified prior to hybridization against a common reference pool of prostate tumor cell lines.
2013-12-23 | E-GEOD-48907 | 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