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Next-generation sequencing facilitates quantitative analysis of miRNAs of cetuximab-resistant colorectal cancer (HCT116-R) cells

ABSTRACT: Next-generation sequencing facilitates quantitative analysis of miRNAs of cetuximab-resistant colorectal cancer (HCT116-R) cells

PROVIDER: PRJNA753592 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15411679.fastq.gz	Fastqsanger.gz
	SRR15411680.fastq.gz	Fastqsanger.gz
	SRR15411681.fastq.gz	Fastqsanger.gz

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Next-generation sequencing facilitates quantitative analysis of miRNAs of cetuximab-resistant colorectal cancer (HCT116-R) cells

Project description:Total RNAs were isolated from three groups, including A group (0×10^9/mL PA-MSHA-treated HCT116 cells), B group (0.3×10^9/mL PA-MSHA-treated HCT116 cells) and C group (0.4×10^9/mL PA-MSHA-treated HCT116 cells). MiRNA sequencing was performed to assess differential expression using next-generation sequencing. The data showed that most miRNAs levels were different in A, B and C groups. Importantly, miR-7-5p was greatly increased in a dose-dependent manner.

2021-08-13 | GSE181843 | GEO

Global gene expression analysis between cetuximab-sensitive and cetuximab-resistant colorectal cancer cells

Project description:Cetuximab is an epidermal growth factor receptor (EGFR)-blocking antibody approved for treatment of metastatic colorectal cancer. We examined differences in global gene expression between the syngeneic DiFi colorectal cancer cells, and a subline of DiFi cells with acquired resistance to cetuximab (DiFi5). We used Affymetrix HG-U133A array to compare the expression pattern of genes that are up-regulated or down-regulated between the parental DiFi colorectal cancer cells and the cetuximab-resistant DiFi5 cells. We generated a cetuximab-resistant DiFi subline, termed DiFi5, by chronic exposure of parental DiFi cells to serially increased doses of cetuximab (from 0.5 nM to 5 nM) for over 1 year. The resulting DiFi5 subline exhibits significant resistance to cetuximab-induced apoptosis. After we confirmed that the phenotype was stable over a period of time of more than 6 months, the RNA from DiFi and DiFi5 cells were extracted and hybridized to an Affymetrix HG-U133A array according to the manufacturerâs instructions. Following the hybridization, the array was scanned using a laser confocal scanner, and microarray image data were analyzed using DNA-Chip Analyzer (dChip), version 1.3, by the Sequencing and Microarray Facility at MD Anderson Cancer Center.

2016-07-17 | E-GEOD-71210 | biostudies-arrayexpress

Global gene expression analysis between cetuximab-sensitive and cetuximab-resistant colorectal cancer cells

2016-07-17 | GSE71210 | GEO

Understanding molecular mechanisms of Cetuximab insensitivity in Colorectal Cancer (CRC)

Project description:Mutational status of KRAS in CRC is used to aid patient stratification for Cetuximab treatment. However, only a subset (10-40%) of patients with wt KRAS respond. We analyzed 40 mCRC tumors for Cetuximab response using a functional ex vivo platform. In the subset of non-responsive tumors, mutational (KRAS/BRAF and PIK3CA) and expression (AREG/EREG) analysis of key genes, transcriptomic profiling and GSEA were carried out to elucidate the molecular mechanisms underlying the response. Our analysis revealed deregulation of multiple pathways, notably Notch and Erbb2 and combined blockade of these two nodes elicited significant antitumor response. These findings collectively indicate the dependence of Cetuximab insensitive mCRC tumors on Notch and Erbb2 for survival and progression. 8 Primary tumors tested in ex vivo platform for response to Cetuximab were subjected to expression analysis

2014-04-01 | E-GEOD-56386 | biostudies-arrayexpress

MicroRNA expression profiling identified miR-31-5p/3p as associated with time to progression in wild-type KRAS metastatic colorectal cancer treated with cetuximab but not panitumumab

Project description:The aim of our study was to investigate whether miRNAs could serve as predictive biomarkers to anti-EGFR therapy (cetuximab, panitumumab) in patients with KRAS wild-type (wt-KRAS) metastatic colorectal cancer (mCRC). In our study, historical cohort of 96 patiens with wt-KRAS mCRC (2006-2009) was included and further divided into exploratory and validation cohorts. Large-scale miRNAs expression profiling was performed on the exploratory cohort of 41 wt-KRAS mCRC patients treated with cetuximab to identify miRNAs associated with time to progression (TTP). The validation was performed on two independent cohorts: 30 patients of wt-KRAS mCRC treated with cetuximab and 25 patients of wt-KRAS mCRC treated with panitumumab.

2016-05-05 | E-MTAB-3548 | biostudies-arrayexpress

Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type HCT116 and MTF1-KO HCT116 injected tumor Transcriptomes

Project description:Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type HCT116 and MTF1-KO HCT116 injected tumor Transcriptomes

| PRJNA787124 | ENA

Understanding molecular mechanisms of Cetuximab insensitivity in Colorectal Cancer (CRC)

2014-04-01 | GSE56386 | GEO

Genomic characterization of intrinsic and acquired resistance to cetuximab in colorectal cancer patients

Project description:Anti-EGFR antibodies are effective in therapies for late-stage colorectal cancer (CRC); however, many tumours are unresponsive or develop resistance. We performed genomic analysis of intrinsic and acquired resistance to anti-EGFR therapy in prospectively collected tumour samples from 25 CRC patients receiving cetuximab (an EGFR inhibitor). Of 25 CRC patients, 13 displayed intrinsic resistance to cetuximab; 12 were intrinsically sensitive. We obtained six re-biopsy samples at acquired resistance from the intrinsically sensitive patients. NCOA4–RET and LMNA–NTRK1 fusions and NRG1 and GNAS amplifications were found in intrinsic-resistant patients. In cetuximab-sensitive patients, we found KRAS K117N and A146T mutations in addition to BRAF V600E, AKT1 E17K, PIK3CA E542K, and FGFR1 or ERBB2 amplifications. The comparison between baseline and acquired-resistant tumours revealed an extreme shift in variant allele frequency of somatic variants, suggesting that cetuximab exposure dramatically selected for rare resistant subclones that were initially undetectable. There was also an increase in epithelial-to-mesenchymal transition at acquired resistance, with a reduction in the immune infiltrate. Furthermore, characterization of an acquired-resistant, patient-derived cell line showed that PI3K/mTOR inhibition could rescue cetuximab resistance. Thus, we uncovered novel genomic alterations that elucidate the mechanisms of sensitivity and resistance to anti-EGFR therapy in metastatic CRC patients.

2019-09-21 | E-MTAB-8340 | biostudies-arrayexpress

Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type HCT116 and MTF1-KO HCT116 injected tumor Transcriptomes

Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to use RNA-seq to find differences between WT and MTF1-KO tumor in colorectal cancer Methods: HCT116 cells and MTF1-KO HCT116 cells were injected subcutaneously into the back of NSG mice at 2x106 cells/recipient , At day 24 after injection，Tumor tissue were isolated from infected recipients，and Total RNA was collected. Besides,about 5x106 cultured HCT116 cells and MTF1-KO HCT116 cells were collected for total RNA isolation ,and sent all of them for sequencing. Conclusions: Our study represents the transcriptome difference between WT HCT116 tumor and MTF1-KO HCT116 tumor has a very positive significance for the pathological process of colorectal cancer，especially for cell adhension

2022-12-15 | GSE190435 | GEO

BCL-xL as a therapeutic target in cetuximab-refractory colorectal cancer

Project description:Despite recent medical advances, colorectal cancer (CRC) remains the second-leading cause of cancer-related death worldwide. For patients with KRAS wild-type metastatic CRC, the monoclonal antibody cetuximab, which targets the epidermal growth factor receptor (EGFR), is an approved treatment option. However, therapeutic success is often limited by the emergence of drug-resistant cancer cell populations within a few months. Therefore, alternative strategies to effectively target cetuximab-refractory CRC are urgently needed. Here, we sought to identify second-line therapeutic strategies using a CRC cell line with acquired cetuximab resistance as a model. Transcriptomic profiling of the resistant cells identified the apoptosis pathway as a potential therapeutic target, which was supported by their increased susceptibility to BH3-mimetics targeting the anti-apoptotic proteins MCL-1 and BCL-xL under both 2D and 3D culture conditions. These findings were validated in organotypic CRC slice cultures generated from cetuximab- resistant patient-derived xenografts (PDXs). Multiplex immunofluorescence staining demonstrated that BCL-xL inhibition effectively triggered apoptosis in heterogeneous PDX tumor slice models, including models harboring oncogenic BRAF mutations. Our findings suggest that cetuximab-resistant CRC retains apoptotic competence, and that BCL-xL inhibition serves as a robust alternative therapeutic strategy that is largely independent of the tumor mutational profile.

2026-01-27 | GSE299943 | GEO

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