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Effect of CRISPR/Cas9 activating library on oxaliplatin resistance during oxaliplatin treatment of HepG2 cells [CRISPR cas9]

ABSTRACT: To identify key drivers of oxaliplatin, Cas9 protein was overexpressed in HepG2 cells. Next, we treated the cell pool with vehicle or OXA for 3 days to enable positive and negative screening

ORGANISM(S): Homo sapiens

PROVIDER: GSE206500 | GEO | 2023/02/28

REPOSITORIES: GEO

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Differentially expressed genes between oxaliplatin-resistant and oxaliplatin-non-resistant patient samples [Clinical samples-RNA-seq]

Project description:To identify key drivers of oxaliplatin resistance, we collected and analyzed the DEGs between oxaliplatin-resistant and oxaliplatin-non-resistant patient samples

2023-02-28 | GSE206501 | GEO

Genome-wide transcriptomic profiling of oxaliplatin response

Project description:Oxaliplatin (OXA) 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 caspase cascade activation through the apoptotic intrinsic pathway. However, not all colon cancer cells show the same sensitivity to OXA. In this study we have compared the changes in RNA expression profiles of colon cancer cell lines with different sensitivity to OXA, determined by IC50.

2011-07-01 | GSE30011 | GEO

Model Establishment of Mice with Oxaliplatin-induced Hepatic Sinusoidal Obstruction Syndrome

Project description:To further explore to mechanisms of oxaliplatin-induced hepatic sinusodial obstruction syndrome, we established a mouse model of OXA-induced HSOS and the difference of mRNA expression level between normal mice and model mice was detected.

2022-09-01 | GSE211859 | GEO

High-throughput sequencing analysis of miRNAs expression profiles in the HCT116 colorectal cancer sublines resistant to oxaliplatin (Oxa) or 5-fluorouracil (5-FU).

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

Pharmacogenomic Approach for the Identification of Novel Determinants of Resistance to Oxaliplatin in Colon Cancer

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

Curcumin mediates oxaliplatin-acquired resistance reversion in colorectal cancer cell lines through modulation of CXC-Chemokine/NF-kB signaling pathway

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

Pharmacogenomic Approach for the Identification of Novel Determinants of Resistance to Oxaliplatin in Colon Cancer

2008-02-07 | GSE10405 | GEO

Minimal genome-wide human CRISPR-Cas9 library.

Project description: Not available

| S-EPMC7818936 | biostudies-literature

Response to oxaliplatin in CCD-18Co

Project description:We obtained the gene expression signature from oxaliplatin-treated fibroblasts and quantified the association of oxaliplatin-activated fibroblasts with disease progression in colorectal cancer.

2023-01-16 | GSE181020 | GEO

Proteomic profile of oxaliplatin treated cell line reveals DNA damage induced nucleolar stress as main response.Proteomic profile of oxaliplatin treated cell line reveals DNA damage induced nucleolar stress as main response

Project description:Oxaliplatin is a widely used anti-cancer drug. It is part of treatment regimens for colorectal and pancreatic cancers, but it is tested in esophageal, biliary tract, gastric or hepatocellular cancers as well. Contrary to this wide application, there is only limited amount of information about oxaliplatin mechanism and response to treatment. We have performed whole-cell proteomic study to obtain cellular response induced by oxaliplatin. For this purpose we have treated CCRF-CEM cell line by 5xIC50 (29.3 μM) for half-time to caspase activation (240 min). The complex proteomic comparison was done on the treated vs. un-treated cells by high-resolution mass spectrometry. We have identified 4049 proteins in average from three biological replicates. From such pool just 76 proteins were significantly downregulated and 31 proteins upregulated in at least of two replicates. Both upregulated and dowregulated proteins are involved in DNA damage response, which is the most significant effect of platinum drugs. Downregulated proteins are split into three fractions. One fraction was centrosomal proteins or proteins involved in G2/M regulation. Second fraction was RNA processing proteins or proteins of processome of both ribosomal subunits. Downregulation of those proteins shows to ongoing nucleolar stress. Third fraction consisted of several ribosomal proteins. This should be sign of ribosomal stress. Nucleolar and ribosomal stress are stress responses manifesting by nucleolar shrinkage or and by inhibition of ribosomal biogenesis. Cellular response to oxaliplatin is thus DNA damage response, which triggers nucleolar and subsequent ribosomal stress.

2017-05-11 | PXD003543 | Pride

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