Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1075029 | ENA |
REPOSITORIES: ENA
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Project description:OXA-48-producing Enterobacterales in dogs feaces
| PRJNA793783 | ENA
Project description:Liver fibrosis is a common pathological process of various chronic liver diseases that can develop into liver cancer. MicroRNAs (miRNAs) are a king of non-coding RNA which are closely related to liver diseases. Thus, this research hope to explore the effect of miR-484 on liver fibrosis and reveal its mechanism. The miRNAs profiles were screened by microRNA sequencing and the location of miR-484 was identified by fluorescence in situ hybridization (FISH) in human liver fibrotic tissues. MiR-484 expression was detected by qRT-PCR in rat primary hepatic stellate cells (HSCs). Bioinformatics analysis and dual-luciferase reporter assay were performed to determine the target gene of miR-484. Liver fibrosis specific signatures were analyzed by qRT-PCR and western blot after miR-484 mimic/inhibitor transfection. The cell apoptosis was detected by Annexin V-FITC/PI double staining. The effect of miR-484 silencing on fibrosis in vivo was investigated in thioacetamide (TAA) induced mice model using the adeno-associated virus carrying miR-484 inhibitor. Enrichment of miR-484 was observed in human liver fibrosis tissues and activated rat primary HSCs. FISH showed that miR-484 was prominently located at fibrotic region and the cytoplasm of HSCs in human liver tissues. Dual-luciferase reporter assay verified that the homeodomain-interacting protein kinases 1 (HIPK1) was the direct target of miR-484. After transfecting miR-484 inhibitor into HSC-T6, HIPK1 were significantly up-regulated, and α-SMA, col1a1, Wnt-3a, Wnt-5a, β-catenin and p-β-catenin were down-regulated, suggesting the restrain effect of miR-484 knockdown on HSCs activation. Conversely, the results were opposite with miR-484 mimic transfection. In addition, the apoptosis of HSC-T6 altered significantly after miR-484 modulation. Moreover, adeno-associated virus carrying miR-484 inhibitor alleviated mice liver fibrosis induced by TAA. In conclusion, miR-484 knockdown ameliorates liver fibrosis by promoting the apoptosis and suppressing HSCs activation via blocking Wnt/β-catenin signaling pathway. MiR-484 and its downstream gene HIPK1 might be selected as novel therapeutic targets of liver fibrosis.
2021-12-09 | GSE190366 | GEO
Project description:Clinical Enterobacterales producing novel OXA-163-like in Argentina
| PRJNA413168 | ENA
Project description:Characterisation of OXA-484, an OXA-48-type carbapenemhydrolysing class D beta-lactamase from E. coli
| PRJNA644256 | ENA
Project description:Resistance to oxaliplatin (OXA) is a complex process affecting the outcomes of metastatic colorectal cancer (CRC) patients treated with this drug. The NF-kBsignalling pathway deregulation has been proposed as an important mechanism involved in this phenomenon. Here, we show that NF-kBwas hyperactivated in in vitro models of OXA-acquired resistance but was attenuated by the addition of Curcumin, a non-toxic NF-kB inhibitor. The concomitant combination of Curcumin+OXA was more effective and synergistic in cell lines with acquired resistance to OXA, leading to the reversion oftheir resistant phenotype, through the inhibition of the NF-kBsignalling cascade. Transcriptomic profiling revealed the up-regulation of three NF-KB-regulated CXC-chemokines, CXCL8, CXCL1 and CXCL2, in the resistant cells thatwere more efficiently down-regulated after OXA+Curcumin treatment as compared to the sensitive cells. Moreover, CXCL8 and CXCL1 gene silencing made resistant cells more sensitive to OXA through the inhibition of the Akt/NF-kBpathway. High expression of CXCL1 in FFPE samples from explant cultures of CRC patients-derived liver metastaseswas associated with response to OXA+Curcumin.In conclusion, we suggest that combination of OXA+Curcumincould be an effective treatment in CRC patients after progression to OXA-based chemotherapy being CXCL1a good candidate predictive marker to this treatment.
2016-12-07 | GSE76092 | GEO
Project description:Oxaliplatin is a member of the family of Pt-containing chemotherapeutic agents that also include cisplatin (CDDP) and carboplatin. OXA is distinguished from these two older drugs by its different spectrum of activity both in preclinical models and in clinical trials. It is the only platinum analogue to have activity in colon cancer, a disease for which this drug has now become a mainstay of therapy. It mainly forms intrastrand adducts between two adjacent guanine residues or guanine and adenine, disrupting DNA replication and transcription. OXA has been reported to be involved in the Nucleotide Excision Repair Pathway (NER), p38 kinase activation, PI3K/AKT pathway and caspases cascade activation through apoptotic intrinsic pathway. However, the downstream molecular events underlying the cytotoxic effects of this chemotherapeutic agent have not been well characterized. This study was developed in order to clarify the multifactoriality of the resistance acquisition process and to identify genes and pathways that could play a role as markers in OXA sensitivity. Keywords: Drug resistance The goal of our experiment was to determine a gene expression profile that discriminates between the OXA-sensitive colorectal cancer cell lines HT29, LoVo, DLD1 and LS513 group and the group of OXA-resistant derived cell lines HTOXAR3, LoVOXAR3, DLDOXAR3 and LSOXAR3 in order to clarify the multifactoriality of the resistance acquisition process and to identify genes and pathways that could play a role as markers in OXA sensitivity. The experimental design used was âRNA-Referenceâ and âDye-Swapâ. Each cell line was analyzed in duplicate, with RNA reference (Stratagene) as reference sample and labeled each biological condition once by Cy3 and once by Cy5. Taking the average of two arrays thus labeled, cancel the dye effect on any particular gene. In total we used 16 slides.
2010-05-26 | E-GEOD-10405 | biostudies-arrayexpress
Project description:In the present study, we investigated miRNA expression changes caused by aquired chemoresistance to 5-FU or Oxa. 40 and 14 miRNAs were detected as differentially expressed in 5-fluouracil- and oxaliplatin-resistant colorectal HCT116 sublines, respectively. Differentially expressed miRNAs determined in the present study could be applied for further development of diagnostic and therapeutic applications for colorectal cancer carcinoma resistant to 5-FU or Oxa.
2019-12-31 | GSE119481 | GEO