Project description:This SuperSeries is composed of the following subset Series:; GSE11550: Hs 294T Cells Treated with Elesclomol Alone or in Combination with Paclitaxel Compared to DMSO Treated; GSE11551: Hs 294T Cells Treated with Elesclomol Alone or in Combination with NAC Compared to DMSO Treated Experiment Overall Design: Refer to individual Series
Project description:We used microarrays to detail gene expression changes in Hs 294T human melanoma cells after treatment with elesclomol alone, or in combination with paclitaxel, to aide in identifing the mechnism of action of elesclomol. Experiment Overall Design: Hs 294T human melanoma cells were grown in vitro. They were seeded at a low density and were left untreated, treated with the vehicle, treated with elesclomol, treated with paclitaxel, or treated in combination with both elesclomol and paclitaxel. They were incubated for 6 hours before harvesting.
Project description:We used microarrays to detail gene expression changes in Hs 294T human melanoma cells after treatment with elesclomol alone, or in combination with paclitaxel, to aide in identifing the mechnism of action of elesclomol. Keywords: treatment
Project description:We used microarrays to detail gene expression changes in Hs 294T human melanoma cells after treatment with elesclomol alone, or in combination with NAC, to aide in identifing the mechnism of action of elesclomol. Experiment Overall Design: Hs 294T human melanoma cells were grown in vitro. They were seeded at a low density and were left untreated, treated with the vehicle, treated with elesclomol, treated with NAC, or treated in combination with both elesclomol and NAC. The cells treated with NAC were given the NAC 30 minutes prior to additional treatments. They were incubated for 6 hours before harvesting.
Project description:We used microarrays to detail gene expression changes in Hs 294T human melanoma cells after treatment with elesclomol alone, or in combination with NAC, to aide in identifing the mechnism of action of elesclomol. Keywords: treatment
Project description:Purpose:Assess the difference in gene expression of taxol-resistant TNBC cells relative to parental cells (MDA-MB-436 and HS 578t) Methods: RNA-seq was performed on paclitaxel-treated MDA-MB-436 cells that are resistant to Paclitaxel (R20A, R20B, R20C) and in control-treated (DMSO) parental MDA-MB-436 cells that are sensitive to Paclitaxel (DMSO) Results: We mapped about 20 million sequence reads per sample to the human genome (hg19) and identified identified differentially expressed genes Conclusions: Our study identified genes significantly enriched or repressed in taxol-resistant cells relative to parental cells in both TNBC models (MDA_MB-436 and HS 578T)
Project description:Glioblastoma (GB) is the most common primary malignant brain tumor, representing approximately 57% of all gliomas and 48% of all primary malignant central nervous system (CNS) tumors. Despite the best standard therapies, glioblastoma survivors have a brief survival time, about 24 months on average. The treatment is troublesome because the cancer cells may not respond well to specific therapies as they grow within an extensive network of blood vessels. A multi-omics approach to provide information on biomolecules from multiple layers appears promising for systematically and holistically understanding complex biology. However, till now, only few studies have utilized omics analysis to investigate the impact of anticancer drugs on GBM. Our study aimed to evaluate the impacts of the anticancer medications (paclitaxel 5.3 μg/mL and topotecan 0.26 μM) solely and in pairwise combination on the metabolic and proteomic signatures of the U87 cell line while utilizing the accurate ultra-high-performance liquid chromatography-electrospray ionization quadrupole time-of-flight mass spectrometry (UHPLC-ESI-QTOF-MS) analytical technology. The studied cancer cells wear treated with DMSO (control group), paclitaxel 5.3 µM, topotecan 0.26 µM, and a combination of paclitaxel 5.3 µM and topotecan 0.26 µM. Using One-way ANOVA, we observed 14 significantly altered metabolites compared to those cells treated with DMSO. For combination treatment (paclitaxel and topotecan), 10 metabolites were significantly dysregulated. The sparse partial least squares-discriminant analysis (sPLS-DA) showed minimal overlapping, indicating a difference between the four groups. While for proteomics, a total of 79 proteins were significantly dysregulated among the groups. These findings can aid in identifying new biomarkers associated with the utilized drugs and creating a map for targeted therapy. EIF3F, GNB2L1, HINT2, and RPA3 were shown to be significantly upregulated in the combination group when compared to the control. Moreover, ribosome, apoptosis, HIF-1 signaling, arginine and proline, glutathione, purine metabolism, apelin signaling pathway, and glycolysis were significantly altered in the combination group.
Project description:Acquired drug resistance represents a major challenge in chemo-therapy treatment for various types of cancers. We have found that the retinoid X receptor–selective agonist bexarotene (LGD1069, Targretin) was efficacious in treating chemo-resistant cancer cells. The goal of this microarray study was to understand the mechanism of bexarotene’s role in overcoming acquired drug resistance using human breast cancer cells MDA-MB-231 as a model system and paclitaxel as model compound. After MDA-MB-231 cells were repeatedly treated with paclitaxel for 8 cycles with each cycle including a 3-day treatment with 30 nM paclitaxel and followed by a 7-day exposure to control medium, MDA cells resistant to paclitaxel were developed and their growth was no longer inhibited by paclitaxel treatment. Those MDA cells with acquired drug resistance, when treated with paclitaxel and bexarotene in combination, could regain their sensitivity and their growth were again inhibited. Therefore, RNA samples from parental MDA-MB-231 cells, paclitaxel-resistant MDA cells treated with vehicle, paclitaxel alone or in combination with bexarotene, were used for perform global gene expression profiling with Affymetrix HG-U133A gene chips. Keywords: Drug Treatment