Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA380111 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:LNCaP prostate cancer cells were treated for 24 hours with either a miRNA negative control (miR-NC) or miRNA 331-3p (miR-331-3p)
2017-03-23 | GSE96918 | GEO
Project description:To determine the altered microRNA expression signature in human prostate cancer compared to benign prostate tissue. To determine the altered mRNA expression signatures upon overexrpession miR-31 in prostate cancer cells. Two condition experiments:1) Total RNA from 21 pairs of prostate cancers and matched benign prostate tissues were collected and processed for microRNA detection. 2) In LNCaP prostate cancer cells, miR-31 was overexpressed and compared to control miR-NC.
2013-02-05 | E-GEOD-36801 | biostudies-arrayexpress
Project description:To determine the altered microRNA expression signature in human prostate cancer compared to benign prostate tissue. To determine the altered mRNA expression signatures upon overexrpession miR-31 in prostate cancer cells. Two condition experiments:1) Total RNA from 21 pairs of prostate cancers and matched benign prostate tissues were collected and processed for microRNA detection. 2) In LNCaP prostate cancer cells, miR-31 was overexpressed and compared to control miR-NC.
2013-02-05 | E-GEOD-36802 | biostudies-arrayexpress
Project description:Purpose: Despite that androgen-deprivation therapy results in long-lasting responses, the disease inevitably progresses to metastatic castration-resistant prostate cancer. In this study, we identified miR-33b-3p as a suppressor of metastasis in prostate cancer. miR-33b-3p was significantly reduced in prostate cancer tissues, and the low expression of miR-33b-3p was correlated with poor overall survival of prostate cancer patients. Overexpression of miR-33b-3p inhibited both migration and invasion of highly metastatic prostate cancer cells whereas antagonizing miR-33b-3p promoted those processes in lowly metastatic cells. The in vivo results demonstrate that miR-33b-3p suppresses metastasis of tail vein inoculated prostate cancer cells to lung, liver, and lymph node in mice. DOCK4 was validated as the direct target of miR-33b-3p. miR-33b-3p decreased the expression of DOCK4 and restoration of DOCK4 could rescue miR-33b-3p inhibition on cell migration and invasion. Moreover, downregulation of miR-33b-3p was induced by bortezomib, the clinically used proteasome inhibitor, and overexpression of miR-33b-3p rescued the insufficient inhibition of bortezomib on migration and invasion in prostate cancer cells. Collectively, our findings demonstrate that miR-33b-3p suppresses metastasis by targeting DOCK4 in prostate cancer. Our results suggest that enhancing miR-33b-3p expression may provide a promising therapeutic strategy for overcoming that proteasome inhibitor’s poor efficacy against metastatic prostate cancer.
2021-09-08 | GSE183428 | GEO
Project description:MicroRNA (miRNA) expression profiles were generated from prostate epithelial sub-populations, enriched from patient-derived benign prostatic hyperplasia (BPH, n=5), Gleason 7 treatment naïve prostate cancer (PCa, n=5) and castration-resistant prostate cancer (CRPC, n=3). Microarray expression was validated in an independent patient cohort (n=10). The analyses show that miRNA expression in epithelial sub-populations (e.g. stem cells) clustered together, irrespective of pathological status. We also discovered concordance between the miRNA expression profiles of unfractioned CRPCs, human embryonic stem cells (SCs), and prostate epithelial SCs (both, benign and malignant). miR-548c-3p was chosen as a candidate miRNA from this group to explore its utility as a CRPC biomarker and/or therapeutic target. Overexpression of miR-548c-3p was confirmed in cancer SCs (8-fold, p<0.05) and unfractionated CRPCs (1.8-fold, p<0.05). Enforced overexpression of miR-548c-3p in differentiated cells induced stem-like properties (p 0.01) and radioresistance (p<0.01). Re-analyses of published studies further revealed that miR-548c-3p is significantly overexpressed in CRPC (p<0.05) and is associated with poor recurrence-free survival (p<0.05), suggesting that miR-548c-3p is a functional biomarker for prostate cancer aggressiveness. Our results validate the prognostic and therapeutic relevance of miRNAs for advanced prostate cancer management, whilst demonstrating that resolving cell-type and differentiation-specific differences is essential to obtain clinical relevant miRNA expression profiles. There are 42 samples in total: 15 benign prostatic hyperplasia, 15 prostate cancers, 9 treatment-resistant prostate cancer. There are stem cells, transit amplifying cells and committed basal cells dissected from each sample. Three PrEC samples of each three cell types can be used as reference.
2016-07-03 | E-GEOD-59156 | biostudies-arrayexpress
Project description:50uM Casodex treatment of LNCaP Prostate Cancer cells
| PRJNA101667 | ENA
Project description:Oxaliplatin (oxPt) resistance in colorectal cancers (CRC) is a major unsolved problem. Consequently, predictive markers and a better understanding of resistance mechanisms are urgently needed. To investigate if the recently identified predictive miR-625-3p is functionally involved in oxPt resistance, stable and inducible models of miR-625-3p dysregulation were analyzed. Ectopic expression of miR-625-3p in CRC cells led to increased resistance towards oxPt. The mitogen-activated protein kinase (MAPK) kinase 6 (MAP2K6/MKK6) – an activator of p38 MAPK - was identified as a functional target of miR-625-3p, and, in agreement, was down-regulated in patients not responding to oxPt therapy. The miR-625-3p resistance phenotype could be reversed by anti-miR-625-3p treatment and by ectopic expression of a miR-625-3p insensitive MAP2K6 variant. Transcriptome, proteome and phosphoproteome profiles revealed inactivation of MAP2K6-p38 signaling as a possible driving force behind oxPt resistance. We conclude that miR-625-3p induces oxPt resistance by abrogating MAP2K6-p38 regulated apoptosis and cell cycle control networks.
2017-03-29 | MSV000080762 | MassIVE
Project description:XMRV is a gammaretrovirus that was thought to be associated with prostate cancer (PC) and chronic fatigue syndrome (CFS) in humans until recently. The virus is culturable in various cells of human origin like lymphocytes, NK cells, neuronal cells, and prostate cell lines. MicroRNAs (miRNAs), which regulate gene expression, were so far not identified in cells infected with XMRV in culture. Two prostate cancer cell lines (LNCaP and DU145) and two primary cells (peripheral blood lymphocytes (PBLs) and monocyte-derived macrophages (MDMs)) were infected with XMRV. Total mRNA was extracted from mock- and virus-infected cells at 6, 24 and 48 hours post-infection and evaluated for microRNA profile in a microarray. MicroRNA expression profiles of XMRV-infected continuous prostate cancer cell lines differ from that of virus-infected primary cells (PBLs and MDMs). miR-193a-3p and miRPlus-E1245 were observed to be specific to XMRV infection in all 4 cell types. While miR-193a-3p levels were down-regulated, miRPlus-E1245 on the other hand exhibited varied expression among the 4 cell types. The present study demonstrates that cellular microRNAs are expressed during XMRV infection of human cells. This is the first report demonstrating the regulation of miR193a-3p and miRPlus-E1245 during XMRV infection in four different human cell types. Two prostate cancer cell lines (LNCaP and DU145) and two primary cells (peripheral blood lymphocytes (PBLs) and monocyte-derived macrophages (MDMs)) were infected with XMRV. Total mRNA was extracted from mock- and virus-infected cells at 6, 24 and 48 hours post-infection in duplicates and evaluated for microRNA profile in a microarray. Each test sample RNA was labeled with Hy3 and the reference pool (made by pooling all 24 test samples in each run) was labeled with Hy5.
2012-05-05 | E-GEOD-37787 | biostudies-arrayexpress
Project description:XMRV is a gammaretrovirus that was thought to be associated with prostate cancer (PC) and chronic fatigue syndrome (CFS) in humans until recently. The virus is culturable in various cells of human origin like lymphocytes, NK cells, neuronal cells, and prostate cell lines. MicroRNAs (miRNAs), which regulate gene expression, were so far not identified in cells infected with XMRV in culture. Two prostate cancer cell lines (LNCaP and DU145) and two primary cells (peripheral blood lymphocytes (PBLs) and monocyte-derived macrophages (MDMs)) were infected with XMRV. Total mRNA was extracted from mock- and virus-infected cells at 6, 24 and 48 hours post-infection and evaluated for microRNA profile in a microarray. MicroRNA expression profiles of XMRV-infected continuous prostate cancer cell lines differ from that of virus-infected primary cells (PBLs and MDMs). miR-193a-3p and miRPlus-E1245 were observed to be specific to XMRV infection in all 4 cell types. While miR-193a-3p levels were down-regulated, miRPlus-E1245 on the other hand exhibited varied expression among the 4 cell types. The present study demonstrates that cellular microRNAs are expressed during XMRV infection of human cells. This is the first report demonstrating the regulation of miR193a-3p and miRPlus-E1245 during XMRV infection in four different human cell types. Two prostate cancer cell lines (LNCaP and DU145) and two primary cells (peripheral blood lymphocytes (PBLs) and monocyte-derived macrophages (MDMs)) were infected with XMRV. Total mRNA was extracted from mock- and virus-infected cells at 6, 24 and 48 hours post-infection in duplicates and evaluated for microRNA profile in a microarray. Each test sample RNA was labeled with Hy3 and the reference pool (made by pooling all 24 test samples in each run) was labeled with Hy5.
2012-05-05 | E-GEOD-37786 | biostudies-arrayexpress
Project description:Treatment-induced neuroendocrine transdifferentiation (NEtD) complicates therapies for metastatic prostate cancer (PCa). We propose that NEtD requires first an intermediary reprogramming to metastable cancer stem-like cells (CSCs) and showed that AR+/PSA+ PCa cell lines were efficiently reprogrammed to and maintained as CSCs by growth in androgen-free neural/neural crest (N/NC) stem medium. Such reprogrammed CSCs overexpressed stem genes, had features of N/NC stem cells, high tumor-initiating potential, resistance to anti-androgen and an EMT phenotype. Serum-containing mediums allowed re-differentiation to N-/NC-derived cell lineages or return back to PCa-like cancer cells. Once returned, the cells had increased resistance to androgen signaling inhibition. Finally, a 62-gene signature derived from reprogrammed PCa cell lines distinguished tumors from PCa patients with adverse outcomes. Gene expression profiles were obtained for RNAs extracted from biological replicates of parental LNCaP cells or from Neuroendocrine-like LNCaP (LNCaP-NE) cells grown for 15 days in CSS-media with no androgen.
2016-03-11 | E-GEOD-66851 | biostudies-arrayexpress