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

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

PROVIDER: PRJNA489366 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7788620_1.fastq.gz	Fastqsanger.gz
	SRR7788620_2.fastq.gz	Fastqsanger.gz
	SRR7788621_1.fastq.gz	Fastqsanger.gz
	SRR7788621_2.fastq.gz	Fastqsanger.gz
	SRR7788622.fastq.gz	Fastqsanger.gz

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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

Screening and molecular mechanism research on bile microRNAs associated with chemotherapy efficacy in perihilar cholangiocarcinoma

Project description:The efficacy of hepatic arterial infusion chemotherapy (HAIC) with oxaliplatin (OXA) and 5-fluorouracil (5-Fu) for treating advanced perihilar cholangiocarcinoma (pCCA) has been demonstrated, yet the survival benefits of HAIC for pCCA patients vary. Here, we aimed to screen out HAIC resistance-related bile microRNAs (miRNAs) and explore the functions of specific bile miRNAs in pCCA based on high-throughput sequencing. Levels of bile miR-532-3p,miR-1250-5p, and miR-4772-5p were related to the survival of advanced pCCA patients after HAIC. However, only overexpression of miR-532-3p promoted OXA/5-Fu resistance, and downregulation of its expression improved sensitivity to OXA/5-Fu. Mechanistic investigations revealed secreted protein acidic and rich in cysteine (SPARC) as the direct target of miR-532-3p. Our study reveals that bile miR-532-3p, miR-1250-5p, and miR-4772-5p may serve as survival biomarkers in advanced pCCA patients after HAIC and that bile miR-532-3p promotes resistance to HAIC with OXA and 5-Fu via negatively regulating SPARC expression.

2024-11-02 | GSE280797 | GEO

Analysis of gene expression profile in 5-fluorouracil (5-FU)-resistant human colon cancer cells

Project description:We analyzed the differentially regulated genes in 5-fluorouracil-resnstant human colon cancer cells to discover novel biomarkers involved in 5-FU resistance in colorectal cancer.

2017-03-27 | GSE56322 | GEO

Novel mechanisms of 5-Fluorouracil Resistance in Colorectal Cancer: A Proteomic Investigation

Project description:One of the main obstacles to therapeutic success in colorectal cancer (CRC) is the development of acquired resistance to treatment with drugs such as 5-fluorouracil (5-FU), the most commonly used drug in CRC patients. Whilst some mechanisms of resistance are well-known, it is clear from the stasis in therapy success rate, that much is still unknown. Here a proteomics approach is taken towards identification using 5-FU resistant sublines of human CRC cell lines generated in-house. Using a multiplexed stable isotope labelling with amino acids in cell culture (SILAC) proteomics strategy, the resistant cell lines, and equivalently passaged 5-FU-sensitive cell lines were compared to parent cell lines grown in Heavy medium using 2D liquid chromatography and Orbitrap Fusion™ Tribrid™ Mass Spectrometry analysis.

2024-06-16 | PXD047672 | Pride

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

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

Pre-treatment metastatic biopsy with response to 5FU and oxaliplatin therapy

Project description:Pre-treatment metastatic (liver) biopsies were harvested prior to 5-FU and oxaliplatin therapy. CT imaging for response evaluation using WHO criteria was performed every 6 weeks.

2011-10-31 | E-MEXP-3368 | biostudies-arrayexpress

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

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