Resistance to antitrypanosomal 2,4-diaminothiazoles
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB55780 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| ERR10175803_1.fastq.gz | Fastqsanger.gz | |||
| ERR10175803_2.fastq.gz | Fastqsanger.gz | |||
| ERR10183204_1.fastq.gz | Fastqsanger.gz | |||
| ERR10183204_2.fastq.gz | Fastqsanger.gz |
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Project description:We used RNAseq to quantify trascript expression from three populations of Conyza sumatrensis before and 5 hours after treatment with 2,4-D. This study investigates different responses between a 2,4-D resistant biotype compared to a 2,4-D sensitive biotype.
2023-06-30 | GSE226337 | GEO
Project description:In the search of new symmetrical derivatives with anticancer activity, we have looked for novel compounds able to induce a selective proapoptotic mechanism in cancer cells. The potential antitumoral activity of several quinazoline derivatives was evaluated in vitro examining their cytotoxic effects against human breast (HTB26), colon (HT29) and bladder (T24) cancer cell lines. Non-tumoral human cell lines were used to test the selectivity of the cytotoxic compounds against cancer cells. Several compounds showed selectivity for cancer cell lines; among them, 2,4-dibencilaminoquinazoline was chosen as the best candidate and its mechanism of action was studied in more detail. This compound was tested for its ability to induce caspase-3 activation and nuclear chromatin degradation in the three cancer cell lines. A time dependent evaluation of apoptosis was performed in the three cancer cell lines, including an expression microarray study at the points of caspase activation and chromatin degradation. 2,4-dibencilaminoquinazoline treatment produces few changes in the expression of genes as evaluated by using microarrays and RT-PCR assays. In conclusion, 2,4-di-p-bromofenilaminoquinazoline is a promising anticancer drug showing cytostatic and apoptotic effects mainly in a transcription independent manner. Keywords: Apoptosis induction, time course
2005-09-21 | GSE3329 | GEO
Project description:Resistance to the phenoxy synthetic auxin herbicide 2,4-D is conferred by a deletion mutation in the degron tail of IAA2. An RNA-Seq experiment was used to assemble a reference transcriptome for the weed species Sisymbrium orientale, to quantify gene expression, and to identify sequence variants in the alignments. A 27 bp deletion was identified in the IAA2 gene. Forward genetics supported the role of this deletion mutation in resistance. The IAA2 deletion allele was transformed into Arabidopsis thaliana to confirm that it conferred 2,4-D resistance.
2020-10-08 | GSE159202 | GEO
Project description:MEK1/2 inhibitors (MEKi) have recently achieved surprising success in treating unresectable plexiform neurofibromas (PNFs). However, few studies have investigated the mechanisms of MEKi resistance in PNF patients. We determined the efficacy of 6 different MEKi for treating PNFs, explored drug resistance mechanisms and identified potential combination therapies to overcome resistance. By screening drug efficacy among 6 MEKi in human NF1-deficient PNF cell lines, TAK-733 was found reduce PNF cell viability the most. We then cultured the TAK-733 resistant cells and explored potential targets for further treatment. Both high-throughput drug screening and RNA sequencing analyses of MEKi-resistant PNF cells identified cyclin-dependent kinase inhibitors (CDKi) as potential agents for PNFs. Dinaciclib, a CDKi, showed synergistic effects on MEKi-resistant cells. Coadministration of dinaciclib and TAK-733 significantly reduced cell viability, inhibited sphere formation and colony formation. Dinaciclib did not affect MEK signaling but decreased the expression of several prosurvival proteins, including survivin and CDK1, to induce apoptosis and inhibit mitosis. TAK-733/dinaciclib combination therapy induced tumor reduction in PNF patient-derived xenografts mouse models. Therefore, the combination of MEKi and CDKi may be promising for treating inoperable PNFs, especially when drug resistance exists. Our findings provide evidence for future clinical trials with MEKi-resistant PNF patients.
2022-05-01 | GSE173577 | GEO
Project description:Background: Current protocols for the treatment of ovarian cancer include combination chemotherapy with a platinating agent and a taxane. However, many patients experience relapse of their cancer and the development of drug resistance is not uncommon, making successful second line therapy difficult to achieve. The objective of this study was to develop a cell line resistant to both carboplatin and docetaxel (dual drug resistant ovarian cell line A2780CBNDXL), along with single agent resistant lines (docetaxel resistant A2780DXL and carboplatin resistant A2780CBN), to investigate the mechanisms which underlie the development of dual drug resistance. Methods: The A2780 epithelial ovarian cancer cell line was used to select for isogenic carboplatin, docetaxel and dual drug resistant cell lines. A selection method of gradually increasing drug doses was implemented to avoid clonal selection. Resistance was confirmed using a clonogenic assay. Changes in gene expression associated with the development of drug resistance were determined by microarray analysis compared to parental co-culture control A2780CC. Changes in selected genes were validated by QPCR and immunoblotting. Results: Three isogenic cell lines were developed and resistance to each drug or the combination of drugs was confirmed. Development of resistance was accompanied by a reduced growth rate. The microarray and QPCR analyses showed that unique changes in gene expression occurred in the dual drug resistant cell line and that genes known to be involved in resistance could be identified in all cell lines. Conclusions: Novel changes in gene expression can occur in the development of dual drug resistance, indicating that dual drug resistance is not a simple combination of the changes occurring in single agent resistance Carboplatin, docetaxel (GSE26129) and carboplatin/docetaxel dual resistant cell lines of ovarian A2780 were generated for gene expression profilling. Two colour microarray of Agilent whole human genome nucleotide arrays was conducted with two replicate of both forward and reverse labellings for each cell line. Four arrays were used for this experiments. And it was four replicate of both forward and reverse labellings for A2780 cells. Eight arrays were used for this experiments
2013-07-22 | E-GEOD-39337 | biostudies-arrayexpress
Project description:Nontarget-site resistance due to rapid physiological response in 2,4-D resistant Conyza sumatrensis: Reduced 2,4-D translocation and auxin-induced gene expression
| PRJNA939725 | ENA
Project description:Background: Current protocols for the treatment of ovarian cancer include combination chemotherapy with a platinating agent and a taxane. However, many patients experience relapse of their cancer and the development of drug resistance is not uncommon, making successful second line therapy difficult to achieve. The objective of this study was to develop a cell line resistant to both carboplatin and docetaxel (dual drug resistant ovarian cell line A2780CBNDXL), along with single agent resistant lines (docetaxel resistant A2780DXL and carboplatin resistant A2780CBN), to investigate the mechanisms which underlie the development of dual drug resistance. Methods: The A2780 epithelial ovarian cancer cell line was used to select for isogenic carboplatin, docetaxel and dual drug resistant cell lines. A selection method of gradually increasing drug doses was implemented to avoid clonal selection. Resistance was confirmed using a clonogenic assay. Changes in gene expression associated with the development of drug resistance were determined by microarray analysis compared to parental co-culture control A2780CC. Changes in selected genes were validated by QPCR and immunoblotting. Results: Three isogenic cell lines were developed and resistance to each drug or the combination of drugs was confirmed. Development of resistance was accompanied by a reduced growth rate. The microarray and QPCR analyses showed that unique changes in gene expression occurred in the dual drug resistant cell line and that genes known to be involved in resistance could be identified in all cell lines. Conclusions: Novel changes in gene expression can occur in the development of dual drug resistance, indicating that dual drug resistance is not a simple combination of the changes occurring in single agent resistance
2013-07-22 | GSE39337 | GEO
Project description:Reliable clinical tests for predicting cancer chemotherapy response are not available and individual markers failed to correctly predict resistance against anticancer agents. We hypothesized that gene expression patterns attributable to chemotherapy-resistant cells can be used as a classification tool for chemoresistance and provide novel candidate genes involved in anthracycline resistance mechanisms. We contrasted the expression profiles of 4 different human tumor cell lines of gastric, pancreatic, colon and breast origin and of their counterparts resistant to the topoisomerase inhibitors daunorubicin or doxorubicin. We also profiled the sensitive parental cells treated with doxorubicin for 24h. We interrogated Affymetrix HGU133A and U95A arrays independently. We applied two independent methods for data normalization and used Prediction Analysis of Microarrays (PAM) for feature selection. In addition, we established data sets related to drug resistance by using a “virtual array” composed of features represented on both types of oligonucleotide arrays. We identified 71 candidate genes associated with doxorubicine/daunorubicine resistance. To validate the microarray data, we also analyzed the expression of 12 selected genes by quantitative RT-PCR or immunocytochemistry, respectively. While the comparison of drug-sensitive versus drug-resistant cells yields candidates associated with drug resistance, the 24h treatment of sensitive parental cells produced a distinct transcriptional profile related to short-term drug effects. Keywords: cell type comparison See Summary. Note: this series includes Affymetrix HGU95A chips (difference between resistant and parental cell lines).
2010-04-15 | E-GEOD-3927 | biostudies-arrayexpress
Project description:Resistance of hypomethylating agents (HMAs) remains a challenge in myelodysplastic neoplasms (MDS), leading to a poor prognosis. Altered metabolism is also reported to be closely associated with drug resistance in hematological malignancies. Here, we conducted a genome-wide CRISPR/Cas9 library screening to identify candidate genes involved in drug sensitivity.
2024-08-05 | GSE273914 | GEO
Project description:Reliable clinical tests for predicting cancer chemotherapy response are not available and individual markers failed to correctly predict resistance against anticancer agents. We hypothesized that gene expression patterns attributable to chemotherapy-resistant cells can be used as a classification tool for chemoresistance and provide novel candidate genes involved in anthracycline resistance mechanisms. We contrasted the expression profiles of 4 different human tumor cell lines of gastric, pancreatic, colon and breast origin and of their counterparts resistant to the topoisomerase inhibitors daunorubicin or doxorubicin. We also profiled the sensitive parental cells treated with doxorubicin for 24h. We interrogated Affymetrix HGU133A and U95A arrays independently. We applied two independent methods for data normalization and used Prediction Analysis of Microarrays (PAM) for feature selection. In addition, we established data sets related to drug resistance by using a “virtual array” composed of features represented on both types of oligonucleotide arrays. We identified 71 candidate genes associated with doxorubicine/daunorubicine resistance. To validate the microarray data, we also analyzed the expression of 12 selected genes by quantitative RT-PCR or immunocytochemistry, respectively. While the comparison of drug-sensitive versus drug-resistant cells yields candidates associated with drug resistance, the 24h treatment of sensitive parental cells produced a distinct transcriptional profile related to short-term drug effects. Keywords: superSeries This reference Series links data in the following related Series: GSE3926 Anthracycline treatment and resistance in four human cancer cell lines (HGU133A) GSE3927 Anthracycline resistance in four human cancer cell lines (HGU95A)
2010-04-14 | E-GEOD-3929 | biostudies-arrayexpress