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S-1 plus Oxaliplatin combination chemotherapy in a stop-and-go fashion for metastatic colorectal cancer

ABSTRACT: Interventions: S-1, Oxaliplatin Primary outcome(s): Frequency and grade of adverse events Study Design: Single arm Non-randomized

DISEASE(S): Metastatic Colorectal Cancer

PROVIDER: 2619539 | ecrin-mdr-crc |

REPOSITORIES: ECRIN MDR

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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

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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.

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METTL3 Confers Oxaliplatin Resistance Through the Activation of G6PD-enhanced Pentose Phosphate Pathway in Hepatocellular Carcinoma

Project description:Oxaliplatin-based therapeutics is a widely used treatment approach for hepatocellular carcinoma (HCC) patients; however, drug resistance poses a significant clinical challenge. Epigenetic modifications have been implicated in the development of drug resistance. In our study, employing siRNA library screening, we identified that silencing the m6A writer METTL3 significantly enhanced the sensitivity to oxaliplatin in both in vivo and in vitro HCC models. Further investigations through combined RNA-seq and non-targeted metabolomics analysis revealed that silencing METTL3 impeded the pentose phosphate pathway (PPP), leading to a reduction in NADPH and nucleotide precursors. This disruption induced DNA damage, decreased DNA synthesis, and ultimately resulted in cell cycle arrest. Mechanistically, METTL3 was found to modify E3 ligase TRIM21 near the 3'UTR with N6-methyladenosine, leading to reduced RNA stability upon recognition by YTHDF2. TRIM21, in turn, facilitated the degradation of the rate-limiting enzyme of PPP, G6PD, through the ubiquitination-proteasome pathway. Importantly, high expression of METTL3 was significantly associated with adverse prognosis and oxaliplatin resistance in HCC patients. Notably, treatment with the specific METTL3 inhibitor, STM2457, significantly improved the efficacy of oxaliplatin. These findings underscore the critical role of the METTL3/TRIM21/G6PD axis in driving oxaliplatin resistance and present a promising strategy to overcome chemoresistance in HCC.

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Differential ncRNAs of oxaliplatin-resistant versus parental HCT116 cells

Project description:Oxaliplatin resistance frequently leads to therapeutic failure in colorectal cancer (CRC). Increasing evidence has shown that noncoding RNAs (ncRNAs) play pivotal roles in chemoresistance of CRC. However, the roles and mechanisms of ncRNAs in oxaliplatin resistance are not well understood. In this study, to identify the ncRNAs induced by oxaliplatin, we profile the expression of ncRNAs in oxaliplatin-resistant HCT116 CRC cells (HCT116oxR) and parental HCT116 cells using next-generation sequencing technology.

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Toxicogenomics profiling of bone marrow from rats treated with topotecan in combination with oxaliplatin: a mechanistic strategy to inform combination toxicity.

Project description:Combinations of anticancer agents may have synergistic anti-tumor effects, but enhanced hematological toxicity often limit their clinical use. We examined whether M-bM-^@M-^\microarray profilesM-bM-^@M-^] could be used to compare early molecular responses following a single dose of agents administered individually with that of the agents administered in a combination. Six patterns of co-expressed genes were detected at the 1-hour time point which indicate regulatory expression of genes dependent on the order of the administration. When topotecan is given first, several signal transduction transcription factors associated with cancer or inactivation of a tumor suppressor were co-regulating gene expression. These results suggest alterations in histone biology, chromatin remodeling, DNA repair, bone regeneration, and respiratory and oxidative phosphorylation are among the prominent pathways modulated in bone marrow from animals treated with an oxaliplatin/topotecan combination. mRNA responses were compared within bone marrow of Sprague-Dawley rats after a single 30-minute treatment with topotecan at 4.7 mg/kg or oxaliplatin at 15 mg/kg alone to that of sequentially administered combination therapy or vehicle control Please note that one of the 'Bone Marrow_Oxaliplatin _Vehicle 1' sample (1344-05H_4M 40) was considered an outlier and thus, was excluded from data analysis and GEO records.

2015-01-21 | E-GEOD-63902 | biostudies-arrayexpress

Difference of gene expression among DLD1, oxaliplatin resistant clones derived from DLD1, HCT116, and oxaliplatin resistant clones derived from HCT116

Project description:Gene expression between DLD1 and DLD1 derived oxaliplatin resistant clones (DLD/OHP1, DLD/OHP4, and DLD/OHP5) was assessed Gene expression between HCT116 and HCT116 derived oxaliplatin resistant clones (HCT/OHP1, HCT/OHP3, and HCT/OHP5) was assessed

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SILAC-Based Quantitative Proteomics Identifies Multifactorial Mechanism of Oxaliplatin Resistance in Pancreatic Cancer Cells

Project description:Oxaliplatin is a commonly used chemotherapeutic drug for the treatment of pancreatic cancer. Understanding the cellular mechanisms of oxaliplatin resistance is important for developing new strategies to overcome drug resistance in pancreatic cancer. In this study, we performed a stable isotope labelling by amino acids in cell culture (SILAC)-based quantitative proteomics analysis of oxaliplatin-resistant and sensitive pancreatic cancer PANC-1 cells. We identified 107 proteins whose expression levels changed between oxaliplatin-resistant and sensitive cells, which were involved in multiple biological processes, including DNA repair, drug response, apoptotic signalling, and the type 1 interferon signalling pathway. Notably, myristoylated alanine-rich C-kinase substrate (MARCKS) and wntless homolog protein (WLS) were upregulated in oxaliplatin-resistant cells compared to sensitive cells, as confirmed by qRT-PCR and Western blot analysis. We further demonstrated the activation of AKT and β-catenin signalling (downstream targets of MARCKS and WLS, respectively) in oxaliplatin-resistant PANC-1 cells. Additionally, we show that the siRNA-mediated suppression of both MARCKS and WLS enhanced oxaliplatin sensitivity in oxaliplatin-resistant PANC-1 cells. Taken together, our results provide insights into multiple mechanisms of oxaliplatin resistance in pancreatic cancer cells and reveal that MARCKS and WLS might be involved in the chemotherapeutic resistance in pancreatic cancer.

2021-09-09 | PXD021251 | Pride

mRNA expression of spinal dorsal horn in oxaliplatin-treated rats

Project description:Oxaliplatin-induced neuropathic pain is a common dose-limiting side effect of cancer treatment but the underlying mechanisms are largely unknown. The neuropathic pain model was established by oxaliplatin intraperitoneal administration for five consecutive days. In the present study, we performed whole genome expression microarray analysis by using spinal dorsal horn from oxaliplatin-treated and vehicle-treated rats on day 10.

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Oxaliplatin mutational signature

Project description:Oxaliplatin mutational signature in HepG2 and MCF10A

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Genome-wide single nucleotide resolution of oxaliplatin-DNA adduct repair in drug sensitive and resistant colorectal cancer cell lines

Project description:Platinum-based chemotherapies, including oxaliplatin, are a mainstay in solid tumor treatment and induce cell death by forming intrastrand dinucleotide DNA adducts. Despite their common use, they are highly toxic and approximately half of patients have tumors that are either intrinsically resistant, or that develop resistance. Studies suggest that this resistance is mediated by variations in DNA repair levels or net drug influx. We aimed to better define the roles of nucleotide excision repair and DNA damage formation in platinum resistance by profiling DNA damage levels and repair efficiency in a panel of seven oxaliplatin-sensitive and three oxaliplatin-resistant colorectal cancer cell lines. We assayed repair indirectly as toxicity, and directly measured bulky adduct formation and removal from the genome by slot blot, repair capacity by excision assay, and mapped repair events genome-wide at single nucleotide resolution using XR-Seq. Using this comprehensive approach of combining novel methods and in some cases using proxies for oxaliplatin-DNA damage, we found no significant difference in repair efficiency that could explain the relative sensitivity and resistance of our cell lines. In contrast, the overall levels of oxaliplatin-DNA damage were significantly lower in resistant cells, indicating that decreased formation of damage, rather than increased repair of that damage, is a major determinant of oxaliplatin resistance. Analysis of gene expression using our XR-seq data showed upregulation of membrane transport pathways in resistant cells, and these pathways may contribute to resistance. Additional research is needed to characterize factors mitigating cellular DNA damage formation by platinum compounds.

2020-05-10 | GSE146473 | GEO

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