Homo sapiens
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PROVIDER: PRJNA376413 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:genome-wide expression profiling of MCF-7, MCF-7/TamR and CAP-treated MCF-7/TamR cell. In result, cold atmospheric plasma re-sensitizes the Tamoxifen-resistant MCF-7 (MCF-7/TamR) breast cancer cell to the drug.
2017-07-12 | GSE95208 | GEO
Project description:Genom-wide expression profiling of MCF-7, MCF-7 and CAP-treated MCF-7 cell. In result, cold atmospheric plasma different effect the CAP-treated MCF-7 breast cancer cell.
2019-07-26 | GSE117491 | GEO
Project description:genom-wide expression profiling of MCF-7, MCF-7 and CAP-treated MCF-7 cell. In result, cold atmospheric plasma different effect the CAP-treated MCF-7 breast cancer cell.
2019-07-26 | GSE110117 | GEO
Project description:Paclitaxel is a widely used therapeutic chemical for breast cancer treatment, however, cancer recurrence remains obstacle for improved prognosis of cancer patients. In the current study, cold atmospheric plasma (CAP) was examined for its potential use to overcome the drug resistance, which mainly comprised of reactive oxygen and nitrogen species. After developing a paclitaxel (Tx)-resistant MCF-7 (MCF-7/TxR) breast cancer cell, CAP was applied to the cells and its effect on recovery of drug sensitivity was examined in cellular as well as molecular aspect. The MCF-7/TxR cells restored sensitivity against Tx up to 70% by CAP. Comparison of genome-wide expression profiles between the Tx resistance cell and its CAP-treated cell identified 86 genes that commonly appeared with significant change. Notably, 48 genes including DAGLA and CEACAM1, which are known to contribute to the acquisition of Tx resistance, showed opposite expression in the two cellular status. The protein expression level of selected genes, DAGLA and CEACAM1, was recovered to that of their parental cell by CAP. Furthermore, the dysregulation of DAGLA and CEACAM1 in MCF-7/TxR alleviated the drug sensitivity recovery effect of CAP. Taken together, CAP inhibited the growth of Tx-resistant MCF-7 cancer cells and recovered Tx sensitivity by resetting expression of multiple drug resistance–related genes. These findings may contribute to extending the application of CAP to the treatment of Tx-resistant cancer.
2020-01-24 | GSE131479 | GEO
Project description:Paclitaxel is a widely used therapeutic chemical for breast cancer treatment, however, cancer recurrence remains obstacle for improved prognosis of cancer patients. In the current study, cold atmospheric plasma (CAP) was examined for its potential use to overcome the drug resistance, which mainly comprised of reactive oxygen and nitrogen species. After developing a paclitaxel (Tx)-resistant MCF-7 (MCF-7/TxR) breast cancer cell, CAP was applied to the cells and its effect on recovery of drug sensitivity was examined in cellular as well as molecular aspect. The MCF-7/TxR cells restored sensitivity against Tx up to 70% by CAP. Comparison of genome-wide expression profiles between the Tx resistance cell and its CAP-treated cell identified 86 genes that commonly appeared with significant change. Notably, 48 genes including DAGLA and CEACAM1, which are known to contribute to the acquisition of Tx resistance, showed opposite expression in the two cellular status. The protein expression level of selected genes, DAGLA and CEACAM1, was recovered to that of their parental cell by CAP. Furthermore, the dysregulation of DAGLA and CEACAM1 in MCF-7/TxR alleviated the drug sensitivity recovery effect of CAP. Taken together, CAP inhibited the growth of Tx-resistant MCF-7 cancer cells and recovered Tx sensitivity by resetting expression of multiple drug resistance–related genes. These findings may contribute to extending the application of CAP to the treatment of Tx-resistant cancer.
2020-01-24 | GSE131478 | GEO
Project description:Paclitaxel is a widely used therapeutic chemical for breast cancer treatment, however, cancer recurrence remains obstacle for improved prognosis of cancer patients. In the current study, cold atmospheric plasma (CAP) was examined for its potential use to overcome the drug resistance, which mainly comprised of reactive oxygen and nitrogen species. After developing a paclitaxel (Tx)-resistant MCF-7 (MCF-7/TxR) breast cancer cell, CAP was applied to the cells and its effect on recovery of drug sensitivity was examined in cellular as well as molecular aspect. The MCF-7/TxR cells restored sensitivity against Tx up to 70% by CAP. Comparison of genome-wide expression profiles between the Tx resistance cell and its CAP-treated cell identified 86 genes that commonly appeared with significant change. Notably, 48 genes including DAGLA and CEACAM1, which are known to contribute to the acquisition of Tx resistance, showed opposite expression in the two cellular status. The protein expression level of selected genes, DAGLA and CEACAM1, was recovered to that of their parental cell by CAP. Furthermore, the dysregulation of DAGLA and CEACAM1 in MCF-7/TxR alleviated the drug sensitivity recovery effect of CAP. Taken together, CAP inhibited the growth of Tx-resistant MCF-7 cancer cells and recovered Tx sensitivity by resetting expression of multiple drug resistance–related genes. These findings may contribute to extending the application of CAP to the treatment of Tx-resistant cancer.
2020-01-24 | GSE131477 | GEO
Project description:Genome wide DNA methylation profiling of estrogene receptor postive breast cancer cell line MCF-7, treating atmospheric cold plasma (plasma). The Illumina Infinium Human Methylation 450k Bead chip was used to obtain DNA methylation profiles across approximately 450,000 CpGs. This profiling indicates that plasma induces epigenetic and cellular changes. Genomic DNA obtained from MCF-7 where effected by cold plasma.
2015-03-31 | E-GEOD-65086 | biostudies-arrayexpress
Project description:Genome wide DNA methylation profiling of estrogene receptor postive breast cancer cell line MCF-7, treating atmospheric cold plasma (plasma). The Illumina Infinium Human Methylation 450k Bead chip was used to obtain DNA methylation profiles across approximately 450,000 CpGs. This profiling indicates that plasma induces epigenetic and cellular changes.
2015-03-31 | GSE65086 | GEO
Project description:Resistance to tamoxifen is a major challenge in the treatment of estrogen receptor positive breast cancer. Acquired resistance to drug involves multilayered genetic and epigenetic regulation . The oncogene EZH2 plays significant role in the development of resistance against tamoxifen, widely used in the treatment of breast cancer. Inhibition of EZH2 has proven to reverse the tamoxifen resistance breast cancer cells back to the sensitive state. The molecular mechanism through which EZH2 inhibition triggers its effects are not known.This study was conducted to understand the global change in proteome profile of tamoxifen resistant MCF-7 breast cancer cells as a result of effect of EZH2 knockdown. Label Free Quantitative proteomics revealed a large number of proteins altered in acquired tamoxifen resistant cells compared to the sensitive cells. A total of 286 proteins were identified with normalized RT for each m/z out of which 86 proteins were upregulated by more than 1.3 fold and 98 proteins were down regulated by more than 1.3 fold in MCF-7 tamoxifen resistant breast cancer cells in comparison to the sensitive breast cancer cells. Upon EZH2 knockdown in tamoxifen resistant cells, a total of 115 proteins were found to be altered with 20 proteins upregulated by more than 1.3 fold and 49 proteins down regulated by more than 1.3 fold. Among the top upregulated proteins were L-lactate dehydrogenase A chain, Alpha and Gamma-enolase, Calreticulin, heat shock protein HSP-90-beta, Alpha-actinin-4, Elongation factor 1-alpha, Vimentin, Protein S100A6, Putative protein FAM10A5, Heterogeneous nuclear ribonucleoprotein A1 and Keratin 1. In addition, 15 proteins were found to be down regulated in EZH2si transfected tamoxifen sensitive cells which otherwise were highlyup regulated in resistant cells in the presence of normal level of EZH2. This indicates a possible regulation of these molecules by EZH2 leading to loss of resistance. Our data unveils important molecular players downstream to EZH2 knockdown leading to regain of sensitivity to tamoxifen in acquired tamoxifen resistance.Thus, EZH2 seems to exert its effects through regulation of metabolism, epithelial to mesenchymal transition and protein synthesis & folding. Hence, targeting EZH2 or the molecules down the cascade might be helpful in reacquiring sensitivity to tamoxifen intamoxifen-resistant cells.
2019-09-30 | PXD012609 | Pride
Project description:Cold atmospheric plasma (CAP) has obtained credits for cancer treatment by its ability to preferentially induce cancer cell death, while its molecular mechanism is under elucidation. Here, an epigenetic effect of CAP on cancer cell was examined by performing a genome-wide ChIP-seq for H3K4me3 in the MCF-7 breast cancer cell.
2019-07-26 | GSE117698 | GEO