Ontology highlight
ABSTRACT:
PROVIDER: PRJNA677979 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13050253_1.fastq.gz | Fastqsanger.gz | |||
| SRR13050253_2.fastq.gz | Fastqsanger.gz | |||
| SRR13050254_1.fastq.gz | Fastqsanger.gz | |||
| SRR13050254_2.fastq.gz | Fastqsanger.gz | |||
| SRR13050255_1.fastq.gz | Fastqsanger.gz |
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Project description:A summary of the work associated to these microarrays is the following: Methotrexate (MTX) is one of the earliest cytotoxic drugs used in cancer therapy, and despite the isolation of multiple other folate antagonists, methotrexate maintains its significant role as a treatment for different types of cancer and other disorders. The usefulness of treatment with methotrexate is limited by the development of drug resistance, which may be acquired through different ways. To get insights into the mechanisms associated with drug resistance and sensitization we have performed a functional analysis of genes deregulated in methotrexate resistant cells, either due to its co-amplification with the DHFR gene or as a result of a transcriptome screening using microarrays. Genes adjacent to dhfr locus and included in the 5q14 amplicon were overexpressed in HT29 MTX-resistant cells. Treatment with siRNAs against those genes caused a slight reduction in cell viability in both HT29 sensitive and resistant cells. On the other hand, microarray analysis of HT29 and HT29 MTX resistant cells unveiled overexpression of caveolin 1, enolase 2 and PKCa genes in treated cells without concomitant copy number gain. siRNAs against these three genes effectively reduced cell viability and caused a decreased MTX resistance capacity. Moreover, overexpression of E-cadherin, which was found underexpressed in MTX-resistant cells, also sensitized the cells toward the chemotherapeutic agent. We provide functional evidences indicating that caveolin 1 and E-cadherin may play a critical role in cell survival and may constitute potential targets for coadjuvant therapy. Keywords: DHFR, Methotrexate, drug resistance
2008-09-08 | GSE11440 | GEO
Project description:A summary of the work associated to these microarrays is the following:; Methotrexate (MTX) is one of the earliest cytotoxic drugs used in cancer therapy, and despite the isolation of multiple other folate antagonists, methotrexate maintains its significant role as a treatment for different types of cancer and other disorders. The usefulness of treatment with methotrexate is limited by the development of drug resistance, which may be acquired through different ways. To get insights into the mechanisms associated with drug resistance and sensitization we have performed a functional analysis of genes deregulated in methotrexate resistant cells, either due to its co-amplification with the DHFR gene or as a result of a transcriptome screening using microarrays. Genes adjacent to dhfr locus and included in the 5q14 amplicon were overexpressed in HT29 MTX-resistant cells. Treatment with siRNAs against those genes caused a slight reduction in cell viability in both HT29 sensitive and resistant cells. On the other hand, microarray analysis of HT29 and HT29 MTX resistant cells unveiled overexpression of caveolin 1, enolase 2 and PKCa genes in treated cells without concomitant copy number gain. siRNAs against these three genes effectively reduced cell viability and caused a decreased MTX resistance capacity. Moreover, overexpression of E-cadherin, which was found underexpressed in MTX-resistant cells, also sensitized the cells toward the chemotherapeutic agent. We provide functional evidences indicating that caveolin 1 and E-cadherin may play a critical role in cell survival and may constitute potential targets for coadjuvant therapy. Experiment Overall Design: Two cell lines are compared in the study, which are HT29 colon cancer cells sensitive to methotrexate and HT29 cells resistant to 10e-5M MTX. Six samples are provided which correspond to triplicated of each cell line. The samples provided were subsequently normalyzed and analyzed using the specific software GeneSpring GX v7.3.1.
2008-10-25 | E-GEOD-11440 | biostudies-arrayexpress
Project description:Using Nanopore sequencing, our study has revealed a close correlation between genomic methylation levels and antibiotic resistance rates in Acinetobacter Baumannii. Specifically, the combined genome-wide DNA methylome and transcriptome analysis revealed the first epigenetic-based antibiotic-resistance mechanism in A. baumannii. Our findings suggest that the precise location of methylation sites along the chromosome could provide new diagnostic markers and drug targets to improve the management of multidrug-resistant A. baumannii infections.
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Project description:Disruption of circadian rhythms is implicated in increasing the risk of cancer development. The Period2 (Per2) gene is one of the major components of mammalian circadian clock, which plays a key role in controlling the circadian rhythms in physiology and behavior. PER2 also has tumor suppression function, but its role in the regulation of susceptibility to chemotherapeutic drugs remains unclear. In this study, we identified up-regulation of Aldehyde dehydrogenase 3a1 (Aldh3a1) gene in oncogenic transformed mouse embryo fibroblasts prepared from Per2-mutant (Per2m/m) mice, which were associated with the resistance against chemotherapeutic drugs. Co-expression of H-rasV12 and SV40 large T antigen induced malignant transformation of both wild-type and Per2m/m cells, but the cytotoxic effects of methotrexate, gemcitabine, etoposide, vincristine, and oxaliplatin were significantly alleviated in oncogenic transformed Per2m/m cells. Although introduction of oncogenes increased the expression of Aldh3a1 in both wild-type and Per2m/m cells, the levels of ALDH3A1 protein in oncogenic transformed Per2m/m cells were 10-fold higher than those in wild-type cells. Elevated ALDH3A1 levels in oncogenic transformed Per2m/m cells were sufficient to prevent chemotherapeutic drug-induced production of reactive oxygen species. Consequently, suppression of Aldh3a1 expression by siRNA relived chemoresistance of Per2m/m cells. These results suggest an uncovered role for PER2 in the development of multiple drug resistance and offers new therapeutic strategies for treatment of cancers.
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Project description:Analysis of metabolic changes in liver from obese mice fed on 60% high fat diet and treated with chemotherapeutic agent methotrexate (50 mg/kg) with a minimum of .
2016-10-07 | GSE87729 | GEO
Project description:Despite the growing understanding about the molecular basis of oncogenesis, prevention and cure of cancer remains an unsurpassed challenge. Chemotherapeutic drugs are the mainstay in managing patients diagnosed with any form of cancer. The emergent chemo-resistance, morbid toxicities and overall inefficacy of current drug portfolios in many cancers necessitate the development of new drugs with novel mechanism of action and selective action on cancer cells. We investigate the molecular action of new chemotherapeutic drug, CLEFMA, uponH441 lund adenocarcinoma cells. The drug was packaged into liposomes and ectopically applied to cells. A control condition comprised from vehicle treated cells. CLEFMA proved to be an effective means of eliminating lung cance rells via oxidative stress induced necrotic cell death. Investigate the effect of new chemotherapeutic drug, CLEFMA. Two groups were compared, five replicates in each group. Control group comprised from cells treated with empty vehicle, test groups was treated with the drug.
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Project description:The aim of this study was to identify biomarkers of drug response and investigate mechanisms of drug resistance to the two chemotherapeutic drugs oxaliplatin and irinotecan (active metabolite SN-38) in colorectal cancer, using a cell-based model system of drug-sensitive parental colon cancer cell lines and sub-cell lines with acquired drug resistance.
2015-03-15 | GSE42387 | GEO
Project description:Malignant pleural mesothelioma (MPM), which is associated with occupational asbestos exposure, is a deadly disease with no effective treatments due mainly to its high resistance to anti-cancer drugs. The molecular mechanisms responsible for its chemotherapeutic resistance are complicated and undefined. However, the presence of side population cells (SP cells) in tumors is a well-accepted explanation for their anti-cancer drug resistance. To identify SP cell-specific gene expression signature, microarray technique has been employed. Our data show differential gene expression profiles between SP and non-SP cells of H2714 mesothelioma cells. SP cells over-expressed genes associated with cancer stem cell (CSC) and drug resistance: DUSP6, SPRY2 and IL6, as well as multi-pathways, including the cancer stem cell-associated pathways Notch and c-Kit. Therefore, we believe that targeting CSC-specific genes and pathways in SP cells may hold the key to the discovery of effective treatments for reversing chemotherapeutic resistance to MPM treatment. 4 samples
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Project description:Tuberculosis (TB) is one of the deadliest infectious disorders in the world. To effectively TB manage, an essential step is to gain insight into the lineage of Mycobacterium tuberculosis (MTB) strains and the distribution of drug resistance. Although the Campania region is declared a cluster area for the infection, to contribute to the effort to understand TB evolution and transmission, still poorly known, we have generated a dataset of 159 genomes of MTB strains, from Campania region collected during 2018-2021, obtained from the analysis of whole genome sequence data. The results show that the most frequent MTB lineage is the 4 according for 129 strains (81.11%). Regarding drug resistance, 139 strains (87.4%) were classified as multi susceptible, while the remaining 20 (12.58%) showed drug resistance. Among the drug-resistance strains, 8 were isoniazid-resistant MTB (HR-MTB), 7 were resistant only to one antibiotic (3 were resistant only to ethambutol and 3 isolate to streptomycin while one isolate showed resistance to fluoroquinolones), 4 multidrug-resistant MTB, while only one was classified as pre-extensively drug-resistant MTB (pre-XDR). This dataset expands the existing available knowledge on drug resistance and evolution of MTB, contributing to further TB-related genomics studies to improve the management of TB infection.
2023-11-17 | E-MTAB-13058 | biostudies-arrayexpress
Project description:Treatment and prophylaxis of the central nervous system (CNS) is a critical component of acute lymphoblastic leukemia (ALL) therapy. However, CNS-directed therapies are a significant cause of morbidity and CNS relapse remains a cause of treatment failure. CNS-directed ALL therapies must target leukemia cells within cerebrospinal fluid (CSF), a fluid that is compositionally distinct from plasma and has been shown to impact leukemia biology. Herein, we demonstrate that human CSF attenuates the potency and efficacy of anti-folate drugs including methotrexate, the primary CNS-directed chemotherapeutic for over six decades. Importantly, this effect of CSF on leukemia methotrexate sensitivity was reversible. Additional mechanistic studies support that diminished proliferation and activation of the integrated stress response (ISR) in leukemia cells in CSF contribute to this resistance. Our findings suggest potential strategies to enhance methotrexate efficacy in CNS-directed ALL therapy and highlight the need to critically reassess even established standards of care.
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