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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE211859 | GEO | 2022/09/01

REPOSITORIES: GEO

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

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

| PRJNA872386 | ENA

Transcription profiling by array of human liver to investigate pathways of Oxaliplatin Related Sinusoidal Obstruction

Project description:Sinusoidal obstruction syndrome (SOS; formerly veno-occlusive disease) is a well-established complication of hematopoietic stem cell transplantation, pyrrolizidine alkaloid intoxication, and widely used chemotherapeutic agents such as oxaliplatin. It is associated with substantial morbidity and mortality. Pathogenesis of SOS in humans is poorly understood. To explore its molecular mechanisms, we used Affymetrix U133 Plus 2.0 microarrays to investigate the gene expression profile of 11 human livers with oxaliplatin-related SOS and compared it to 12 matched controls. Hierarchical clustering analysis showed that profiles from SOS and controls formed distinct clusters. To identify functional networks and gene ontologies, data were analyzed by the Ingenuity Pathway Analysis Tool. A total of 913 genes were differentially expressed in SOS: 613 being upregulated and 300 downregulated. Reverse transcriptase-PCR results showed excellent concordance with microarray data. Pathway analysis showed major gene upregulation in six pathways in SOS compared with controls: acute phase response (notably interleukin 6), coagulation system (Serpine1, THBD, and VWF), hepatic fibrosis/hepatic stellate cell activation (COL3a1, COL3a2, PDGF-A, TIMP1, and MMP2), and oxidative stress. Angiogenic factors (VEGF-C) and hypoxic factors (HIF1A) were upregulated. The most significant increase was seen in CCL20 mRNA. In conclusion, oxaliplatin-related SOS can be readily distinguished according to morphologic characteristics but also by a molecular signature. Global gene analysis provides new insights into mechanisms underlying chemotherapy-related hepatotoxicity in humans and potential targets relating to its diagnosis, prevention, and treatment. Activation of VEGF and coagulation (vWF) pathways could partially explain at a molecular level the clinical observations that bevacizumab and aspirin have a preventive effect in SOS. This dataset is part of the TransQST collection.

2012-01-18 | E-MTAB-503 | biostudies-arrayexpress

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

Project description: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

2023-02-28 | GSE206500 | 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

AKR1C1 Drives Oxaliplatin Chemoresistance by Activation of STAT3 in Colorectal Cancer

Project description:AKR1C1, a member of the AKR1C family, has been identified as a key player in cancer progression, promoting cancer cell proliferation and inhibiting apoptosis. Here, we identified AKR1C1 as a potential crucial gene significantly associated with oxaliplatin (OXA) sensitivity and unfavorable clinical outcomes through the transcriptome analysis of OXA-sensitive and -resistant colorectal cancer cell lines. Both in vitro and in vivo, AKR1C1 promotes cancer cell proliferation and confers OXA chemoresistance in colorectal cancer cells. Mechanistically, AKR1C1 interacts with and activates STAT3 and increases glutathione (GSH) levels, resulting in chemoresistance in colorectal cancer cells. Moreover, pharmacologic inhibition of AKR1C1 with alantolactone restores the sensitivity of resistant cell lines to OXA and the combined treatment of alantolactone with OXA exhibits superior antitumor effects in mouse xenografts. Collectively, the present study offers compelling evidence that AKR1C1 expression confers resistance to OXA in colorectal cancer, providing a promising strategy to circumvent chemoresistance.

2024-12-11 | GSE235026 | GEO

Identification of molecular pathways involved in oxaliplatin-associated sinusoidal dilatation

Project description:Oxaliplatin-based chemotherapy for colorectal liver metastases (CRLM) can result in vascular liver lesions such as sinusoidal dilatations. Physiopathology remains unclear and variability between patients suggests that there is individual susceptibility. A better understanding of the molecular mechanisms of oxaliplatin liver toxicity may allow to identification of biomarkers and adaptation of chemotherapy delivery. non-tumor frozen liver samples were obtained from patients operated on for CRLM after an exclusive oxaliplatin-based chemotherapy. Gene-expression profiles were first analyzed by microarray on a selected population of 20 patients; 9 patients with severe sinusoidal dilatation (SD) after a short period of chemotherapy and 10 patients without any sinusoidal dilatation after a long period of chemotherapy. These were compared with a control group of 5 patients without any chemotherapy and lesions. This dataset is part of the TransQST collection.

2012-03-01 | E-GEOD-32384 | biostudies-arrayexpress

Prevention of the Hepatic Sinusoidal Obstruction Syndrome by Means of Anticoagulants

Project description:The purpose of the study is to determine whether anticoagulant use (i.e. salicylates, clopidogrel, low-molecular weight heparin, or coumarin derivates) is able to prevent the development of the sinusoidal obstruction syndrome secondary to oxaliplatin-based neoadjuvant chemotherapy in patients suffering from colorectal liver metastases.

| 2071144 | ecrin-mdr-crc

Identification of molecular pathways involved in oxaliplatin-associated sinusoidal dilatation

2012-03-01 | GSE32384 | 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

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