Arsenic hexoxide has differential effects on cell proliferation and genome-wide gene expression in human primary mammary epithelial and MCF7 cells
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ABSTRACT:
PROVIDER: PRJNA661769 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12601577_1.fastq.gz | Fastqsanger.gz | |||
| SRR12601577_2.fastq.gz | Fastqsanger.gz | |||
| SRR12601578_1.fastq.gz | Fastqsanger.gz | |||
| SRR12601578_2.fastq.gz | Fastqsanger.gz | |||
| SRR12601579_1.fastq.gz | Fastqsanger.gz |
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Project description:Arsenic is reportedly a biphasic inorganic compound for its toxicity and anticancer effects in humans. Recent studies have shown that certain arsenic compounds including arsenic hexoxide_x000D_ (AS4O6; hereafter, AS6) induce programmed cell death and cell cycle arrest in human cancer cells and murine cancer models. However, the mechanisms by which AS6 suppresses cancer cells are incompletely understood. In this study, we show markedly differential effects of AS6 on cytotoxicity and gene expression in human mammary epithelial normal cells (HUMEC) and Michigan Cancer Foundation 7 (MCF7), a human mammary epithelial cancer cell line. AS6 selectively arrests cell growth and induces cell death in MCF7 cells without affecting the growth of HUMEC in a dose-dependent_x000D_ manner. AS6 alters the transcription of a large number of protein-coding genes in MCF7 cells, but much fewer genes in HUMEC. Importantly, we found that the cell proliferation, cell cycle, and DNA repair pathways are significantly suppressed whereas cellular stress response and apoptotic pathways_x000D_ increase in AS6-treated MCF7 cells. Together, we provide the first evidence of differential effects of AS6 on normal and cancerous breast epithelial cells, suggesting that AS6 at moderate concentrations induces cell cycle arrest and apoptosis through modulating genome-wide gene expression, leading to compromised DNA repair and increased genome instability selectively in human breast cancer cells
2021-02-17 | GSE157574 | GEO
Project description:Arsenic is reportedly a biphasic inorganic compound for its toxicity and anticancer effects in humans. Recent studies have shown that certain arsenic compounds including arsenic hexoxide (AS4O6; hereafter, AS6) induce programmed cell death and cell cycle arrest in human cancer cells and murine cancer models. However, the mechanisms by which AS6 suppresses cancer cells are incompletely understood. In this study, we report the mechanisms of AS6 through transcriptome analyses. In particular, the cytotoxicity and global gene expression regulation by AS6 were compared in human normal and cancer breast epithelial cells. Using RNA-sequencing and bioinformatics analyses, differentially expressed genes in significantly affected biological pathways in these cell types were validated by real-time quantitative polymerase chain reaction and immunoblotting assays. Our data show markedly differential effects of AS6 on cytotoxicity and gene expression in human mammary epithelial normal cells (HUMEC) and Michigan Cancer Foundation 7 (MCF7), a human mammary epithelial cancer cell line. AS6 selectively arrests cell growth and induces cell death in MCF7 cells without affecting the growth of HUMEC in a dose-dependent manner. AS6 alters the transcription of a large number of genes in MCF7 cells, but much fewer genes in HUMEC. Importantly, we found that the cell proliferation, cell cycle, and DNA repair pathways are significantly suppressed whereas cellular stress response and apoptotic pathways increase in AS6-treated MCF7 cells. Together, we provide the first evidence of differential effects of AS6 on normal and cancerous breast epithelial cells, suggesting that AS6 at moderate concentrations induces cell cycle arrest and apoptosis through modulating genome-wide gene expression, leading to compromised DNA repair and increased genome instability selectively in human breast cancer cells.
| S-EPMC7881197 | biostudies-literature
Project description:These RNA-seq data were generated to correlate with genomic interaction data in a related Hi-C analysis. MCF10A is a normal-like mammary epithelial cell line and MCF7 is a transformed estrogen responsive breast cancer cell line derived from a metastatic site; both are commonly used in models of breast cancer progression. Analysis revealed a set of genes related to repression of WNT signalling that were both up-regulated in MCF7 and located in genomic regions that had transitioned from closed to open structure in MCF7.
2015-09-02 | GSE71862 | GEO
Project description:These RNA-seq data were generated to correlate with genomic interaction data in a related Hi-C analysis. MCF10A is a normal-like mammary epithelial cell line and MCF7 is a transformed estrogen responsive breast cancer cell line derived from a metastatic site; both are commonly used in models of breast cancer progression. Analysis revealed a set of genes related to repression of WNT signalling that were both up-regulated in MCF7 and located in genomic regions that had transitioned from closed to open structure in MCF7. RNA-seq of MCF10A and MCF7 cells. 3 replicates each. Sequencing was strand-specific and conducted on ribo-depleted RNA.
2015-09-02 | E-GEOD-71862 | biostudies-arrayexpress
Project description:MicroRNAs are widely expressed in the normal pubertal mammary gland and orchestrate mammary gland development by regulating cell proliferation, differentiation, apoptosis, and metabolism. Although human Growth hormone(hGH) plays fundamental roles in normal mammary gland development and elevated autocrine hGH levels have been documented to contribute to breast cancer, whether hGH should influence the expression pattern and the functional roles of miRNAs in this context remain unknown.This study explores the effects of autocrine hGH on microRNA expression in MCF7 cell.
2014-12-31 | GSE58845 | GEO
Project description:The effects of several compounds on the MCF7 human adenocarcinoma mammary cell line were analysed by gene expression profiling.
2010-07-14 | GSE19638 | GEO
Project description:Using a large variety of methods we demostrate that PGR can be a driver of tumor proliferation even in absence of extensive E2. In this specific experiment we treat MCF7 cells intraductally xenografted into the ductal tree of a mouse mammary gland, with estrogen (E2), progesterone (P4) and the combination of the two (E2+P4).
2022-04-05 | GSE192809 | GEO
Project description:In our earlier study, thiourea has been shown to improve the growth of rice and reduce the arsenic load from aerial parts of the seedlings. We have also shown the applicability of thiourea to delineate the redox regulatory mechansisms under arsenic stress in rice. To move further, present microarray was performed to reveal the involvement of overall gene and regulatory netwrok under arsenic with/without thiourea treatment in rice.
2015-09-15 | GSE71492 | GEO
Project description:Arsenic is a carcinogen that is known to induce cell transformation and tumor formation. Although studies have been performed to examine the modulation of signaling molecules caused by arsenic exposure, the molecular mechanisms by which arsenic causes cancer are still unclear. We hypothesized that arsenic alters gene expression leading to carcinogenesis in the lung. In this study, we examined global gene expression in response to 0.75 µM arsenic treatment for 1-7 days in a rat lung epithelial cell line (L2) using an in-house 10k rat DNA microarray. One hundred thirty one genes were identified using the one-class statistical analysis of microarray (SAM) test. Of them, 33 genes had a fold change of ≥ 2 at least between two time points. These genes were then clustered into 5 groups using K-means cluster analysis based on their expression patterns. Seven selected genes, all associated with cancer, were confirmed by real-time PCR. These genes have functions directly or indirectly related to metabolism, glycolysis, cell proliferation and differentiation, and regulation of transcription, all of which may be involved in neoplastic transformation of cells. Our findings provide important insight for the future studies of arsenic-mediated lung cancer. Keywords: Lung, aresenic, L2, micorarray
2011-12-23 | GSE9790 | GEO
Project description:In our earlier study, thiourea has been shown to improve the growth of rice and reduce the arsenic load from aerial parts of the seedlings. We have also shown the applicability of thiourea to delineate the redox regulatory mechansisms under arsenic stress in rice. To move further, present microarray was performed to reveal the involvement of overall gene and regulatory netwrok under arsenic with/without thiourea treatment in rice. Agilent custom one-color experiment,Organism:Oryza sativa, Whole Genome Rice 8x60k (AMADID: 064722) designed by Genotypic Technology Private Limited.
2015-09-15 | E-GEOD-71492 | biostudies-arrayexpress