Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1059612 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR27393000.fastq.gz | Fastqsanger.gz | |||
| SRR27393001.fastq.gz | Fastqsanger.gz | |||
| SRR27393002.fastq.gz | Fastqsanger.gz | |||
| SRR27393003.fastq.gz | Fastqsanger.gz | |||
| SRR27392992.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 12 |
Similar Datasets
Project description:The dataset analyzed in the report entitled Plasma extracellular vesicle microRNAs reflecting the therapeutic effect of the CBP/β-catenin inhibitor PRI-724 in patients with liver cirrhosis
2024-03-20 | GSE250272 | GEO
Project description:Plasma extracellular vesicle (EV) miRNA profile before and after the administration of PRI-724 in patients with liver cirrhosis
2024-03-20 | GSE250179 | GEO
Project description:Plasma extracellular vesicle microRNAs reflecting the therapeutic effect of the CBP/β-catenin inhibitor PRI-724 in patients with liver cirrhosis
| PRJNA1052615 | ENA
Project description:Wnt/β-catenin is involved in every aspect of embryonic development and in the pathogenesis of many human diseases, and is also implicated in organ fibrosis. However, the role of β-catenin-mediated signaling on liver fibrosis remains unclear. To explore this issue, the effects of PRI-724, a selective inhibitor of the cAMP-response element-binding protein-binding protein (CBP)/β-catenin interaction, on liver fibrosis were examined using carbon tetrachloride (CCl4)- or bile duct ligation (BDL)-induced mouse liver fibrosis models. Following repetitive CCl4 administrations, the nuclear translocation of β-catenin was observed only in the non-parenchymal cells in the liver. PRI-724 treatment reduced the fibrosis induced by CCl4 or BDL, accompanied by the suppression of S100A4 expression, a CBP/β-catenin transcript. C-82, an active form of PRI-724, inhibited the activation of isolated primary mouse quiescent hepatic stellate cells (HSCs) and promoted cell death in culture-activated HSCs. During the fibrosis resolution period, an increase in F4/80+ CD11b+ and Ly6Clow CD11b+ macrophages was induced by CCl4 and was sustained for two weeks thereafter, even after having stopped CCl4 treatment. PRI-724 accelerated the resolution of CCl4-induced liver fibrosis, and this was accompanied by increased matrix metalloproteinase (MMP)-9, MMP-2, and MMP-8 expression in intrahepatic leukocytes. These results suggest that the inhibition of CBP/β-catenin suppresses liver fibrosis through the inhibition of HSCs activation, the induction of activated HSC death, and the production of MMPs from macrophages. Thus, targeting the CBP/β-catenin interaction may become a new therapeutic strategy in treating liver fibrosis. We used microarrays to detail the global change of gene expression by PRI-724 (C-82)-treatment in culture-activated murine hepatic stellate cells.
2018-09-30 | GSE73603 | GEO
Project description:Survivin, the member of the inhibitors of apoptosis (IAP) protein family is overexpressed in various cancer types while remaining nearly undetectable in normal cells. Survivin overexpression is associated with increased chemotherapy resistance, tumor recurrence, and shorter patient survival. Bioinformatics analysis supported the observation that increased expression of survivin may be a biomarker of poorer patients’ survival and may contribute to resistance to standard targeted therapy of melanoma. The lack of identifiable active sites and enzymatic activity make targeting survivin challenging. Therefore, indirect targeting of survivin may represent a feasible therapeutic approach. To downregulate survivin, we used PRI-724, an inhibitor of CBP/β-catenin signaling axis. While PRI-724 has demonstrated efficacy in preclinical models and clinical trials in different cancer types, its potential in melanoma had not been previously assessed. Treatment of drug-naïve, trametinib- and vemurafenib-resistant melanoma cells with PRI-724 was sufficient to downregulate survivin and other CBP/β-catenin target proteins, inhibit proliferation, reduce invasiveness and induce apoptosis. These findings indicated that PRI-724 exhibited significant antitumor activity in both drug-naïve melanoma cells and their drug-resistant counterparts. Among the resistant populations, trametinib-resistant melanoma cells showed the greatest sensitivity to PRI-724 treatment, whereas vemurafenib-resistant melanoma cells, which exhibited the higher expression of survivin, were the less responsive to PRI-724 treatment.
2025-09-30 | GSE301849 | GEO
Project description:This randomized phase II trial studies how well combination chemotherapy and bevacizumab with or without CBP/beta-catenin antagonist PRI-724 (PRI-724) works in treating patients with newly diagnosed colorectal cancer that has spread to other places in the body. Drugs used in chemotherapy, such as leucovorin calcium, oxaliplatin, and fluorouracil, work in different ways to stop the growth of tumor cells, either by killing the cells, by stopping them from dividing, or by stopping them from spreading. Monoclonal antibodies, such as bevacizumab, may block tumor growth in different ways by targeting certain cells. PRI-724 may help stop the growth of cancer cells by blocking the specific signaling pathway that cancer cells need to grow and spread. It is not yet known whether combination chemotherapy and bevacizumab works better with or without PRI-724 in treating patients with metastatic colorectal cancer.
| 2187697 | ecrin-mdr-crc
Project description:The development of resistance to platinum-based chemotherapy remains the unsurmountable obstacle in cancer treatment and consequently leads to tumor relapse. This study aims to investigate the mechanism by which loss of RBMS3 induced chemoresistance in epithelial ovarian cancer (EOC). Experimental design: Fluorescence in situ hybridization and immunochemistry were used to determine deletion frequency and expression of RBMS3 in 15 clinical EOC tissues and 150 clinicopathologically characterized EOC specimens. The effects of RBMS3 deletion and CBP/β-catenin antagonist PRI-724 in chemoresistance were examined by clone formation and Annexin V assays in vitro, and by intraperitoneal tumor model in vivo. The mechanism by which RBMS3 loss sustained activation of miR-126-5p/β-catenin/CBP signaling and the effects of RBMS3 and miR-126-5p competitively regulating DKK3, AXIN1, BACH1 and NFAT5 was explored using CLIP-seq (PRJNA484809), RIP, electrophoretic mobility shift and immunoblotting immunofluorescence assays. Results: Loss of RBMS3 in EOC was correlated with the overall and relapse-free survival. Genetic ablation of RBMS3 significantly enhanced, whereas restoration of RBMS3 reduced, the chemoresistance ability of EOC cells both in vitro and in vivo. RBMS3 inhibited β-catenin/CBP signaling through directly associating with and stabilizing multiple negative regulators, including DKK3, AXIN1, BACH1 and NFAT5, via competitively preventing the miR-126-5p-mediated repression of these transcripts. Importantly, co-therapy of CBP/β-catenin antagonist PRI-724 induced sensitization of RBMS3-deleted EOC to platinum therapy. Conclusions: Our results demonstrate that genetic ablation of RBMS3 contributes to chemoresistance and PRI-724 may serve as a potential tailored treatment for patients with RBMS3-deleted EOC.
2018-11-06 | GSE122146 | GEO
Project description:The major obstacle to human immunodeficiency type 1 (HIV-1) eradication is a reservoir of latently-infected cells that persists despite long-term antiretroviral therapy (ART) and is maintained through cellular proliferation. Long-lived memory CD4+ T-cells with high self-renewal capacity such as central memory T-cells (CM) and T memory stem cells (SCM) are major contributors to the viral reservoir in HIV-infected individuals on ART. The Wnt/β-catenin signaling pathway regulates the balance between self-renewal and differentiation of SCM and CM T-cells and pharmacological manipulation of this pathway offers an opportunity to interfere with the proliferation of latently-infected cells. Here, we evaluated in vivo a novel approach to inhibit self-renewal of SCM and CM CD4+ T-cells in the rhesus macaque (RM) model of SIV infection. We used an inhibitor of the Wnt/β-catenin pathway, PRI-724, that blocks the interaction between the co-activator CREB binding protein (CBP) and β-catenin, resulting in the cell fate decision to differentiate rather than proliferate. Our study shows that PRI-724 treatment of ART-suppressed SIVmac251-infected RMs: (i) was well tolerated, with blood counts, liver enzymes, and renal function within normal limits and no alteration of tri-lineage hematopoiesis observed in bone marrow, (ii) resulted in decreased proliferation of SCM and CM T-cells, (iii) modified the SCM and CM CD4+ T-cell transcriptome towards a profile of more differentiated memory T-cells, and (iv) reduced SIV-DNA levels in CM and TFH CD4+ T-cells in the lymph nodes, but did not decrease the overall viral reservoir size. This work is the first demonstration in vivo that pharmacological modulation can effectively target T cell stemness in long-lived memory CD4+ T-cells, and represents a potential strategy to reduce HIV persistence.
2022-02-24 | GSE127330 | GEO
Project description:Extracellular Vesicle and Particle miRNAs in Maternal Plasma
| PRJNA925502 | ENA