Comparison of H460 derived CSCs and cisplatin-resistant cells
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE54981 | GEO | 2014/07/30
SECONDARY ACCESSION(S): PRJNA238197
REPOSITORIES: GEO
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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: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: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.
2011-09-27 | GSE21656 | GEO
Project description:Cancer Stem Cells derived from human non-small cells lung cancer (NSCLC) H460 cells were differentiated by culturing them in the presence of Foetal Bovine Serum under adherent conditions. Changes in gene expression profiles were determined at 3, 9 and 24 hours of differentiation
2014-07-30 | GSE54712 | GEO
Project description:Cancer Stem Cells derived from from human non-small cells lung cancer (NSCLC) H460 cells were differentiated by culturing them in the presence of Foetal Bovine Serum under adherent conditions. Changes in gene expression profiles were determined at 3, 9 and 24 hours of differentiation Expression profiles were determined for H460C cells undifferentiated of after 3, 9 and 24 hours of differentiation. Each sample type was hybridized to in-situ oligonucleotide microarrays (Agilent-014850 Whole Human Genome Microarray 4x44K). One channel per slide. Each differentiated population was compared to undifferentiated cells. Biological replicates: 2
2014-07-30 | E-GEOD-54712 | biostudies-arrayexpress
Project description: Not available
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Project description:DUSP1 is involved in different cellular pathways including cancer cell proliferation, angiogenesis, invasion and resistance to chemotherapy. To gain insight into the cellular signaling pathways involving DUSP1 actions and the response to Cisplatin (CDDP) in non small cell lung cancer (NSCLC), we have used a double strategy that combines microarray and SiRNA technology. This strategy provided a differential expression profile of genes involved in CDDP response in NSCLC cell line regulated by DUSP1 using H460 and H460cri and a time course to CDDP. KEYWORDS: Expression profiling by array in cells with genetic modification in response to CCDP treatment
2012-01-01 | GSE26704 | GEO
Project description:DUSP1 is involved in different cellular pathways including cancer cell proliferation, angiogenesis, invasion and resistance to chemotherapy. To gain insight into the cellular signaling pathways involving DUSP1 actions and the response to Cisplatin (CDDP) in non small cell lung cancer (NSCLC), we have used a double strategy that combines microarray and SiRNA technology. This strategy provided a differential expression profile of genes involved in CDDP response in NSCLC cell line regulated by DUSP1 using H460 and H460cri and a time course to CDDP. KEYWORDS: Expression profiling by array in cells with genetic modification in response to CCDP treatment The human non small lung cancer cell line H460 used in this study was from ATCC (American Type Culture Collection). The cell line was maintained in RPMI (Gibco, Invitrogen) supplemented with 10% bovine serum and transfected by Lipofectamine Plus Reagent from Life Technologies as directed by the manufacturer. The DUSP1 pSuperRetro-derived vectors were constructed as described (Chattoppadhyay et al., 2006). Clones expressing siRNA for DUSP1 were selected for their ability to grow in the presence of puromycin and kept for selection. Stable transfection was confirmed by Western blotting. We analyzed the differences in expression of 47000 genes in H460 cells expressing DUSP1SiRNA (H460cri) compared with the parental cell line H460pSuperRetro vector (H460v) after 0, 1, 3 and 6 hours of CDDP exposure, in order to know the different pathways that were activated by CDDP treatment dependent on expression of DUSP1. RNA was extracted and quality control was checked before hybridization on Affymetrix microarrays.
2012-01-01 | E-GEOD-26704 | biostudies-arrayexpress
Project description:We generated H460 cells with acquired TRAIL resistance by exposing the parental sentisitve cells to subtoxic concentrations of TRAIL for 6 months. Then we compared the gene expression profile of the sensitive versus the resistant cells. We generated acquired TRAIL-resistant H460 cells from the sentisitve cells by treating subtoxic range of TRAIL for 6 month. And we tried to compare the expressional profile of the genes between two cell types to isolate genes regulating acquired TRAIL-resistance H460 cells were treated with subtoxic concentrations of TRAIL for 6 month. After confirmation of the resistance, the RNA was extracted and the gene expression profile was analyzed.
2014-09-01 | E-GEOD-55859 | biostudies-arrayexpress
Project description:We generated H460 cells with acquired TRAIL resistance by exposing the parental sentisitve cells to subtoxic concentrations of TRAIL for 6 months. Then we compared the microRNA expression profile in the sensitive versus resistant cells. H460 cells were treated with subtoxic concentrations of TRAIL for 6 month. After confirmation of the resistance, the RNA was extracted and the microRNA expression profile was analyzed using the NanoString technology.
2014-09-01 | E-GEOD-55821 | biostudies-arrayexpress