Drug treatment comparison
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Se Nyun Kim
PROVIDER: E-GEOD-2182 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:H460 cells were treated with 5-FU, cytarabin, cisplatin, paclitaxel, and cytochalasin D. Gene expression changes induced by drug treatment were compared. Keywords: other
2005-01-27 | GSE2182 | GEO
Project description:Background: Drug resistance by epigenetic modulation in cancer cells has been suggested, and the epigenetic-driven heterogeneity has been suggested as an important mechanism. To elucidate the epigenetic mechanism further, epigenetically reprogrammed cancer (R-cancer) cells were established and their resistance during differentiation was analyzed. Methods: R-cancer cells for H460 (R-H460) were established by transient introduction of reprogramming factors. Then, differentiated R-H460 (dR-H460) cells were prepared by withdrawal of stem cell media (SCM) for various durations, and the changes in drug resistance were tested. Results: dR-H460 cells with SCM-withdrawal for about 2 weeks (mdR-H460 cells) formed significantly more drug-resistant colonies to both cisplatin and paclitaxel. The resistant phenotype of the cisplatin resistant colonies from mdR-H460 cells, however, was lost after long-term (about 70-90 days) cisplatin-withdrawal, suggesting a transient epigenetic mechanism. In another R-cancer cell model with N87, the increased drug-resistance was also observed for both cisplatin and paclitaxel after SCM-withdrawal. In single cell analyses, heterogeneity did not increase significantly in mdR-H460, although relatively higher fraction of mdR-H460 cells was observed in several clusters of parent H460 cells. Conclusion: Based on R-cancer model, increased cancer cell population under epigenetic transition, rather than heterogeneity from epigenetic changes, may confer the epigenetic-driven drug resistance, which can provide a new strategy to fight cancers by control of cancer cells under epigenetic transition.
2020-10-22 | GSE139275 | GEO
Project description:Transcription profile of cancer stem cells isolated from human non-small cells lung cancer (NSCLC) H460 cells. The profile of H460 cells that were made resistant to cisplatin after a single treatment with the drug was also determined. Both profiles were finally compared. Each microarray contained one of these comparative experiments (two-channels): H460C (H460 derived CSCs) vs H460 and H460R (cisplatin-resistant H460 cells) vs H460. Technical replicates were made with dye-swap-based design. Total biological replicates per cell type (H460C and H460R): 2.
2014-07-30 | E-GEOD-54981 | biostudies-arrayexpress
Project description:Anticancer drug clustering in lung cancer based on gene expression profiles. We performed gene expression analysis in lung cancer cell lines. (used: Affymetrix GeneChip Human Genome U133 Array Set HG-U133A). We also examines the sensitivity of these cell lines to commonly used anti-cancer agents (docetaxel, paclitaxel, gemcitabine, vinorelbine, 5-FU, SN38, cisplatin, and carboplatin) via MTT assay. We related the cytoxic activity of each of these agents to corresponding expression pattern in each of the cell lines using modified NCI program. Keywords: cytotoxicity, lung cancer, anticancer drugs
2006-02-10 | GSE4127 | GEO
Project description:Transcription profile of cancer stem cells isolated from human non-small cells lung cancer (NSCLC) H460 cells. The profile of H460 cells that were made resistant to cisplatin after a single treatment with the drug was also determined. Both profiles were finally compared.
2014-07-30 | GSE54981 | GEO
Project description:The FITExP profiling approach was used to identify protein hits from cells incubated with RAPTA-T or RAPTA-EA. Validation experiments with paclitaxel and cisplatin underlined the reliability of the method and hit lists for both test compounds (and?) gave physiologically viable anti-cancer mechanisms. The hit proteins for paclitaxel match with those published and the ones obtained for cisplatin were related to DNA repair, which is in line with the principal mechanism of cisplatin cytotoxicity involving the formation of nuclear DNA lesions. RAPTA-T treatment leads to upregulation of multiple hits suggesting a broad mechanism of action involving both metastasis and tumorigenicity. In contrast, hit proteins identified after incubation with RAPTA-EA are linked to regulation of the oxidative stress response and are therefore thought to be conferred by the EA moiety in the drug. From a therapeutic standpoint, RAPTA-EA could be explored in cancers where EA alone has shown potency, such as chronic lymphocytic leukemias,91 or where EA combined with another agent shows synergy, such as the combination of EA with afatinib, an irreversible epidermal growth factor receptor tyrosine kinase inhibitors for breast cancers.92 On the other hand, due to its broad mechanism of action, RAPTA-T could potentially be more useful if used concomitantly with drugs that target specific cancer pathways and could also play a role in therapies for later stage cancers due to its anti-metastatic properties. Here, application of the FITExP allowed us to gauge the mechanistic pathways involved in the action of two novel ruthenium(II) metallodrugs with very different phenotypic characteristics and from this knowledge infer their role in therapy. Potentially, future application of the FITExP approach in this manner could be useful for identification of cancer chemotherapy drug combinations, where commonly cancer clinical trials fail at phase II where drug combinations are first tried and tested.
2018-02-09 | PXD005766 | Pride
Project description:Anticancer drug clustering in lung cancer based on gene expression profiles. We performed gene expression analysis in lung cancer cell lines. (used: Affymetrix GeneChip Human Genome U133 Array Set HG-U133A). We also examines the sensitivity of these cell lines to commonly used anti-cancer agents (docetaxel, paclitaxel, gemcitabine, vinorelbine, 5-FU, SN38, cisplatin, and carboplatin) via MTT assay. We related the cytoxic activity of each of these agents to corresponding expression pattern in each of the cell lines using modified NCI program. Experiment Overall Design: gene expression analysis in lung cancer cell lines
2007-12-12 | E-GEOD-4127 | biostudies-arrayexpress
Project description:Protein profile changes of glioma cells treated with temozolomide or albumin-bound paclitaxel were screened by proteomics
2023-03-28 | PXD041176 | iProX
Project description:Combination of platinum-based chemotherapy and radiation is currently the standard treatment for locally advanced lung cancer patients. However, therapeutic resistance to these therapies may arise from the presence of cancer stem cells (CSCs). To investigate the CSCs hypothesis of chemo-radiation resistance, we used microarray assay to profile CSCs-like cisplatin-resistant lung cancer cells (CDDP-R) versus its parental cells. CDDP-R cells were established by exposing H460 lung cancer cells to 3µM cisplatin for 7 days, followed by 0.8% methylcellulose selection over 14 consecutive days. We found that CDDP-R cells expressed higher levels of stem cell markers, including CD133 and ALDH. They are more resistant to cisplatin- and etoposide-induced apoptosis and to high radiation dose (20Gy). Clonogenic assays suggest that CDDP-R cells were more resistant to radiation than parental H460 cells (DER=1.21, p<0.01). Xenograft studies suggest that CDDP-R cells were more tumorigenic (p<0.001). Microarray and comprehensive protein interaction networks analyses revealed IGFBP3 as a highly ranked hub protein which plays an important role in the mechanism of cisplatin resistance. We found reduced level of IGFBP3 and enhanced IGFR-1 activation upon IGF stimulation in CDDP-R cells. The specific targeting of IGF-1R using siRNA resulted in significant sensitization of CDDP-cells (DER=1.17, p<0.05) to radiation compared with the parental H460 cells. Our findings suggest that CDDP-R cells have the characteristics of CSCs and constitute a “suitable” model to study lung CSCs. Profiling of CSCs-like H460 cells led to the identification of IGF as an important pathway for chemo- and radiotherapy resistance in lung cancer. gene expression comparison of two groups
2011-09-26 | E-GEOD-21656 | biostudies-arrayexpress
Project description:Partial response to chemotherapy leads to disease resurgence. Upon treatment, a subpopulation of cancer cells, called drug-tolerant persistent cells, displays a transitory drug tolerance that lead to treatment resistance. Though drug-tolerance mechanisms remain poorly known, they have been linked to non-genomic processes, including epigenetics, stemness and dormancy. 5-fluorouracil (5-FU), the most widely used chemotherapy in cancer treatment, is associated with resistance. While prescribed as an inhibitor of DNA replication, 5-FU alters all RNA pathways. Here, we show that 5-FU treatment leads to the unexpected production of fluorinated ribosomes, exhibiting altered mRNA translation. 5-FU is incorporated into ribosomal RNAs of mature ribosomes in cancer cell lines, colorectal xenografts, and human tumors. Fluorinated ribosomes appear to be functional, yet, they display a selective translational activity towards mRNAs according to the nature of their 5'-untranslated region. As a result, we found that sustained translation of IGF-1R mRNA, which codes for one of the most potent cell survival effectors, promoted the survival of 5-FU-treated colorectal cancer cells. Altogether, our results demonstrate that "man-made" fluorinated ribosomes favour the drug-tolerant cellular phenotype by promoting translation of survival genes. This could be exploited for developing novel combined therapies. By unraveling translation regulation as a novel gene expression mechanism helping cells to survive a drug-challenge, our study extends the spectrum of molecular mechanisms driving drug-tolerance.
2021-06-25 | GSE178839 | GEO