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:50uM Casodex treatment of LNCaP Prostate Cancer cells
| PRJNA101667 | ENA
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: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: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:Siomycin A treatment in prostate cancer cell lines PC3 and LNCaP
| PRJNA153401 | ENA
Project description:mRNA expression upon reconstitution of miR-130a, miR-203 and miR-205 in prostate cancer cell line LNCaP
| PRJNA123603 | ENA
Project description:Study the function of miR-195 and miR-30d in prostate cancer cell (LNCap and DU145)
| PRJNA339681 | ENA