Expression profiling of ovarian cancer cell lines
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Ed Curry
PROVIDER: E-GEOD-41499 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:Paired platinum-sensitive & platinum-resistant cell lines PEO1 and PEO4 (respectively) were derived from the same patient. Cell line cultures were profiled with the HT-HGU133a GeneChip to investigate chemotherapy resistance related expression of genes marked with different histone modifications in a primary ovarian tumour (clinical data for the primary ovarian tumour is available as Series supplementary file).
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Project description:This SuperSeries is composed of the following subset Series: GSE41498: Profiling of ovarian tumour and benign lesions GSE41499: Expression profiling of ovarian cancer cell lines Refer to individual Series
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2008-06-16 | E-GEOD-8193 | biostudies-arrayexpress
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2008-11-13 | E-GEOD-10061 | biostudies-arrayexpress
Project description:Background: Tumor heterogeneity is one of the key factors leading to chemo-resistance relapse. It remains unknown how resistant cancer cells influence sensitive cells during cohabitation and growth within a heterogenous tumors. The goal of our study was to identify driving factors that mediate the interactions between resistant and sensitive cancer cells and to determine the effects of cohabitation on both phenotypes. Methods: We used isogenic ovarian cancer cell (OC) lines pairs, sensitive and resistant to platinum: OVCAR5 vs. OVCAR5 CisR and PEO1 vs. PEO4, respectively, to perform long term direct culture and to study the phenotypical changes of the interaction of these cells. Results: Long term direct co-culture of sensitive and resistant OC cells promoted proliferation (p < 0.001) of sensitive cells and increased the proportion of cells in the G1 and S cell cycle phase in both PEO1 and OVCAR5 cells. Direct co-culture led to a decrease in the IC50 to platinum in the cisplatin-sensitive cells (5.92 µM to 2.79 µM for PEO1, and from 2.05 µM to 1.51 µM for OVCAR5). RNAseq analysis of co-cultured cells showed enrichment of Cell Cycle Control, Cyclins and Cell Cycle Regulation pathways. The transcription factor E2F1 was predicted as the main effector responsible for the transcriptomic changes in sensitive cells. Western blot and qRT-PCR confirmed upregulation of E2F1 in co-cultured vs monoculture. Furthermore, an E2F1 inhibitor reverted the increase in proliferation rate induced by co-culture to baseline levels. Conclusions: Our data suggest that long term cohabitation of platinum-sensitive and -resistant cancer cells drive sensitive cells to a higher proliferative state, more responsive to platinum. Our results reveal an unexpected effect caused by direct interactions between cancer cells with different proliferative rates and levels of platinum resistance, modelling competition between cells in heterogeneous tumors.
2024-02-11 | GSE244626 | GEO
Project description:Changes in chromatin organization are associated with resistance to anti-cancer drugs, such as platinum-based chemotherapy used as the primary treatment of ovarian cancer. We have examined the genomic distribution of chromatin accessibility changes, and relationship to gene expression changes, occurring during acquisition of resistance in vivo of high grade serous ovarian cancer (HGSOC) patients and whether this associates with genomic DNA damage distribution. Using matched chemo-sensitive and chemo-resistant ovarian cell lines isolated from HGSOC patients before and following acquisition of clinical resistance to platinum-based chemotherapy, we have examined the relationship between chromatin accessibility by ATAC-seq, platinum-DNA adduct distribution by Pt-Exo-seq and gene expression by RNA-seq. We have correlated chromatin changes between the lines at gene promoters, CpG islands, enhancer sequences and other genomic regions with changes in gene expression and platinum-DNA adduct distribution. We observe chromatin conformation differences following acquisition of platinum-resistance, with the HGSOC resistant lines clustering together, separately from their respective sensitive counterparts. Resistant lines show altered chromatin accessibility at intergenic regions, but less so at gene promoters. Super-enhancers, as defined by clusters of cis-regulatory elements, at these intergenic regions show chromatin changes that are associated with altered expression of linked genes, with enrichment for genes involved in the Fanconi anemia/BRCA DNA damage response pathway. Genome-wide distribution of platinum adducts associates with the chromatin changes and distinguish sensitive from resistant lines. Regions incurring fewer platinum-adducts showed a significant reduction in accessibility the resistant HGSOC cell line PEO4 compared to the sensitive PEO1 counterpart. Surprisingly, regions showing increased damage in PEO4 had an even greater reduction in accessibility. In the resistant line, we observe fewer adducts around gene promoters and more adducts at intergenic regions. In cell lines derived from patients following acquisition of clinical resistance to platinum-based chemotherapy, chromatin changes at super-enhancers correlate with gene expression changes in DNA repair pathways known to influence platinum sensitivity. Although cisplatin is a relatively non-specific DNA damaging agent, there are consistent differences in distribution of adducts between the matched sensitive and resistant ovarian cell lines, which is independent of the overall level of adducts formed.
2021-03-27 | GSE149146 | GEO
Project description:Changes in chromatin organization are associated with resistance to anti-cancer drugs, such as platinum-based chemotherapy used as the primary treatment of ovarian cancer. We have examined the genomic distribution of chromatin accessibility changes, and relationship to gene expression changes, occurring during acquisition of resistance in vivo of high grade serous ovarian cancer (HGSOC) patients and whether this associates with genomic DNA damage distribution. Using matched chemo-sensitive and chemo-resistant ovarian cell lines isolated from HGSOC patients before and following acquisition of clinical resistance to platinum-based chemotherapy, we have examined the relationship between chromatin accessibility by ATAC-seq, platinum-DNA adduct distribution by Pt-Exo-seq and gene expression by RNA-seq. We have correlated chromatin changes between the lines at gene promoters, CpG islands, enhancer sequences and other genomic regions with changes in gene expression and platinum-DNA adduct distribution. We observe chromatin conformation differences following acquisition of platinum-resistance, with the HGSOC resistant lines clustering together, separately from their respective sensitive counterparts. Resistant lines show altered chromatin accessibility at intergenic regions, but less so at gene promoters. Super-enhancers, as defined by clusters of cis-regulatory elements, at these intergenic regions show chromatin changes that are associated with altered expression of linked genes, with enrichment for genes involved in the Fanconi anemia/BRCA DNA damage response pathway. Genome-wide distribution of platinum adducts associates with the chromatin changes and distinguish sensitive from resistant lines. Regions incurring fewer platinum-adducts showed a significant reduction in accessibility the resistant HGSOC cell line PEO4 compared to the sensitive PEO1 counterpart. Surprisingly, regions showing increased damage in PEO4 had an even greater reduction in accessibility. In the resistant line, we observe fewer adducts around gene promoters and more adducts at intergenic regions. In cell lines derived from patients following acquisition of clinical resistance to platinum-based chemotherapy, chromatin changes at super-enhancers correlate with gene expression changes in DNA repair pathways known to influence platinum sensitivity. Although cisplatin is a relatively non-specific DNA damaging agent, there are consistent differences in distribution of adducts between the matched sensitive and resistant ovarian cell lines, which is independent of the overall level of adducts formed.
2021-03-27 | GSE149145 | GEO
Project description:Changes in chromatin organization are associated with resistance to anti-cancer drugs, such as platinum-based chemotherapy used as the primary treatment of ovarian cancer. We have examined the genomic distribution of chromatin accessibility changes, and relationship to gene expression changes, occurring during acquisition of resistance in vivo of high grade serous ovarian cancer (HGSOC) patients and whether this associates with genomic DNA damage distribution. Using matched chemo-sensitive and chemo-resistant ovarian cell lines isolated from HGSOC patients before and following acquisition of clinical resistance to platinum-based chemotherapy, we have examined the relationship between chromatin accessibility by ATAC-seq, platinum-DNA adduct distribution by Pt-Exo-seq and gene expression by RNA-seq. We have correlated chromatin changes between the lines at gene promoters, CpG islands, enhancer sequences and other genomic regions with changes in gene expression and platinum-DNA adduct distribution. We observe chromatin conformation differences following acquisition of platinum-resistance, with the HGSOC resistant lines clustering together, separately from their respective sensitive counterparts. Resistant lines show altered chromatin accessibility at intergenic regions, but less so at gene promoters. Super-enhancers, as defined by clusters of cis-regulatory elements, at these intergenic regions show chromatin changes that are associated with altered expression of linked genes, with enrichment for genes involved in the Fanconi anemia/BRCA DNA damage response pathway. Genome-wide distribution of platinum adducts associates with the chromatin changes and distinguish sensitive from resistant lines. Regions incurring fewer platinum-adducts showed a significant reduction in accessibility the resistant HGSOC cell line PEO4 compared to the sensitive PEO1 counterpart. Surprisingly, regions showing increased damage in PEO4 had an even greater reduction in accessibility. In the resistant line, we observe fewer adducts around gene promoters and more adducts at intergenic regions. In cell lines derived from patients following acquisition of clinical resistance to platinum-based chemotherapy, chromatin changes at super-enhancers correlate with gene expression changes in DNA repair pathways known to influence platinum sensitivity. Although cisplatin is a relatively non-specific DNA damaging agent, there are consistent differences in distribution of adducts between the matched sensitive and resistant ovarian cell lines, which is independent of the overall level of adducts formed.
2021-03-27 | GSE147645 | GEO