Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA147341 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Short hairpin RNA library-based functional screening identified ribosomal protein L31 that modulates prostate cancer cell growth
2015-05-15 | GSE60382 | GEO
Project description:Short hairpin RNA library-based functional screening identified ribosomal protein L31 that modulates prostate cancer cell growth Vehicle vs. bicalutamide treated LNCaP cells infected with lentiviral shRNA library. Biological replicates: 2 vehicle treatments, 2 bicalutamide treatments.
2015-05-15 | E-GEOD-60382 | biostudies-arrayexpress
Project description:Recovery of hairpins targeting a known prostate cancer pathway testing the utility of shRNA library screening in prostate cancer as a broad strategy to identify new candidate drug targets.
2012-08-31 | GSE32261 | GEO
Project description:Prostate cancer is the most common cancer in men and AR downstream signalings promote prostate cancer cell proliferation. To investigate the AR signaling, we performed short RNA sequence analysis in AR positive prostate cancer cell line, LNCaP. In addition, we used hormone-refractory prostate cancer model cells, Bicalutamide-resistant (BicR) to explore the differences of androgen signaling in prostate cancer progression. Short RNA sequence analysis of androgen-regulated miRNAs in two prostate cancer cells
2015-09-01 | E-GEOD-66035 | biostudies-arrayexpress
Project description:An increasing number of cancer-associated mutations have been identified. Unfortunately, little therapy today exploits these tumor-specific genetic lesions. Often, the resulting oncoproteins have been intractable to easy manipulation with current small molecule screening approaches. To overcome this impasse, we developed an expression-based approach to small molecule library screening. We applied this platform to the discovery of modulators of the activity of EWS/FLI, the Ewing sarcoma associated oncoprotein. Cytarabine (ARA-C) was identified as the top hit in a small molecule library screen. ARA-C modulates EWS/FLI by decreasing EWS/FLI protein level and has striking effects on cellular viability and transformation in in vitro and in vivo models of Ewing sarcoma. With poor outcomes for patients with relapsed Ewing sarcoma and the well established safety profile of ARA-C, clinical trials testing ARA-C in Ewing sarcoma are warranted. Expression data was created for A673 cells treated with ARA-C and two other compounds used to treat Ewing sarcoma (Puromycin and Doxorubicin) at two doses (EC50 and 2xEC50) and three time points (24 hours, 3 days, and 5 days). Keywords: time course and dose response
2007-03-01 | GSE6930 | GEO
Project description:Recovery of hairpins targeting a known prostate cancer pathway testing the utility of shRNA library screening in prostate cancer as a broad strategy to identify new candidate drug targets. Two cell lines assayed for 4 time points with a control and 2 experimental conditions. Two to four replicates of each instance are provided.
2012-08-31 | E-GEOD-32261 | biostudies-arrayexpress
Project description:Background: G-quadruplex (G4) structures are important epigenetic regulators and potential therapeutic targets in cancer. However, their role in prostate cancer, particularly in relation to the immune microenvironment, remains poorly understood. Methods: We performed BG4 ChIP_x001E_seq to map genome_x001E_wide G4 structures in the prostate cancer cell line C4_x001E_2. Bioinformatics analyses integrated G4_x001E_associated genes with immune pathway enrichment and machine learning algorithms (LASSO, SVM_x001E_RFE, GBM, Naïve Bayes, and GLM) to identify hub genes in prostate cancer progression. Clinical data from GTEx, TCGA, and HPA were analyzed for expression and survival. Functional validation included qPCR, CCK_x001E_8, colony formation, and wound_x001E_healing assays. Druggability was assessed using DrugnomeAI, and AI_x001E_assisted peptide design was performed with RFdiffusion and ProteinMPNN. Results: We identified 1289 prostate cancer_x001E_specific G4 structures, predominantly in promoter regions. Machine learning and immune enrichment analysis pinpointed IKBKB as a key hub gene in prostate cancer progression. IKBKB was overexpressed in prostate cancer tissues, correlated with advanced stage and poor prognosis, and was regulated by promoter G4 structures via transcription factors AR and ERG. IKBKB promoted genome instability, tumor stemness, and immune microenvironment remodeling. G4 stabilization increased IKBKB expression and activated the NF_x001E_κB pathway, enhancing cancer cell viability, proliferation, and migration. Computational screening confirmed IKBKB’s druggability and identified potential inhibitors (e.g., Auranofin). AI_x001E_assisted design generated peptide inhibitors targeting IKBKB and a CRISPR_x001E_dCas9 strategy for G4 disruption.
2026-06-03 | GSE334282 | GEO
Project description:Prostate cancer is the most common cancer in men and AR downstream signalings promote prostate cancer cell proliferation. To investigate the AR signaling, we performed RNA sequence analysis in AR positive prostate cancer cell line, LNCaP. In addition, we used hormone-refractory prostate cancer model cells, Bicalutamide-resistant (BicR) to explore the differences of androgen signaling in prostate cancer progression. Short RNA sequence analysis of androgen-regulated miRNAs in two prostate cancer cells
2015-09-01 | E-GEOD-66036 | biostudies-arrayexpress
Project description:An increasing number of cancer-associated mutations have been identified. Unfortunately, little therapy today exploits these tumor-specific genetic lesions. Often, the resulting oncoproteins have been intractable to easy manipulation with current small molecule screening approaches. To overcome this impasse, we developed an expression-based approach to small molecule library screening. We applied this platform to the discovery of modulators of the activity of EWS/FLI, the Ewing sarcoma associated oncoprotein. Cytarabine (ARA-C) was identified as the top hit in a small molecule library screen. ARA-C modulates EWS/FLI by decreasing EWS/FLI protein level and has striking effects on cellular viability and transformation in in vitro and in vivo models of Ewing sarcoma. With poor outcomes for patients with relapsed Ewing sarcoma and the well established safety profile of ARA-C, clinical trials testing ARA-C in Ewing sarcoma are warranted. Expression data was created for A673 cells treated with ARA-C and two other compounds used to treat Ewing sarcoma (Puromycin and Doxorubicin) at two doses (EC50 and 2xEC50) and three time points (24 hours, 3 days, and 5 days). Experiment Overall Design: A673 cells were treated with ARA-C (at doses of EC50 and 2xEC50) or vehicle in triplicate and expression profiled at 24 hours, 3 days, and 5 days. To exclude the possibility that ARA-C's modulation of the EWS/FLI signature was simply a non-specific response to treatment with all cytotoxic agents, we asked whether other compounds known to kill Ewing sarcoma cells (Doxorubicin and Puromycin) would induce the EWS/FLI off genome-wide expression pattern. A673 cells were treated with Doxorubicin and Puromycin (at doses of EC50 and 2xEC50) and expression profiled at 24 hours, 3 days, and 5 days.
2008-11-22 | E-GEOD-6930 | biostudies-arrayexpress