Homo sapiens isolate:MCF7 | breed:Cell Line
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ABSTRACT:
PROVIDER: PRJNA703307 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:In this study, we reporte the altered miRNAs expression in the human breast cancer cell line (MCF7) derived mammosphere in response to withaferin A IC50 concentrations (2 µM)..
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Project description:Small RNA next generation sequencing of miRNAs in MCF7 cells derived mammosphere treated with withaferin A
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Project description:Ell3 is a RNA polymerase II transcription elongation factor that is enriched in testis. The C-terminal domain of Ell3 shows strong similarities to that of Ell (eleven-nineteen lysine-rich leukemia gene), which acts as a negative regulator of p53 and regulates cell proliferation and survival. Recent studies in our laboratory showed that Ell3 induces the differentiation of mouse embryonic stem cells by protecting differentiating cells from apoptosis via the promotion of p53 degradation. In this study, we evaluated the function of Ell3 in breast cancer cell lines. MCF7 cell lines overexpressing Ell3 were used to examine cell proliferation and cancer stem cell properties. Ectopic expression of Ell3 in breast cancer cell lines induces proliferation and 5-FU resistance. In addition, Ell3 expression increases the cancer stem cell population, which is characterized by CD44 (+) or ALDH1 (+) cells. Mammosphere-forming potential and migration ability were also increased upon Ell3 expression in breast cancer cell lines. Through biochemical and molecular biological analyses, we showed that Ell3 regulates proliferation, cancer stem cell properties and drug resistance in breast cancer cell lines partly through the MEK-extracellular signal-regulated kinase signaling pathway. Murine xenograft experiments showed that Ell3 expression promotes tumorigenesis in vivo. The transcription elongation factor Ell3 induces chemosensitization of MCF7 cells to the chemotherapeutic agent cis-diamminedichloroplatinum (II) (CDDP) by stabilizing p53. Interestingly, Ell3 induced p53 stabilization in response to CDDP by promoting binding of p53 to NADH quinoneoxidoreductase 1 (NQO1), which is linked to an ubiquitin-independent degradation pathway, as well as by suppressing a MDM2 mediated ubiquitin-dependent degradation pathway. Furthermore, Ell3 enhanced interleukin-20 (IL-20) expression leading to the activation of the ERK1/2 signaling pathway. By analyzing the suppressive effects of IL-20 and ERK signaling in the Ell3 expressing MCF7 cells, we confirmed that the IL-20 mediated ERK1/2 signaling pathway is the main cause of p53 stabilization after CDDP exposure in MCF7 cells.
2015-11-25 | GSE63612 | GEO
Project description:Ell3 is a RNA polymerase II transcription elongation factor that is enriched in testis. The C-terminal domain of Ell3 shows strong similarities to that of Ell (eleven-nineteen lysine-rich leukemia gene), which acts as a negative regulator of p53 and regulates cell proliferation and survival. Recent studies in our laboratory showed that Ell3 induces the differentiation of mouse embryonic stem cells by protecting differentiating cells from apoptosis via the promotion of p53 degradation. In this study, we evaluated the function of Ell3 in breast cancer cell lines. MCF7 cell lines overexpressing Ell3 were used to examine cell proliferation and cancer stem cell properties. Ectopic expression of Ell3 in breast cancer cell lines induces proliferation and 5-FU resistance. In addition, Ell3 expression increases the cancer stem cell population, which is characterized by CD44 (+) or ALDH1 (+) cells. Mammosphere-forming potential and migration ability were also increased upon Ell3 expression in breast cancer cell lines. Through biochemical and molecular biological analyses, we showed that Ell3 regulates proliferation, cancer stem cell properties and drug resistance in breast cancer cell lines partly through the MEK-extracellular signal-regulated kinase signaling pathway. Murine xenograft experiments showed that Ell3 expression promotes tumorigenesis in vivo. The transcription elongation factor Ell3 induces chemosensitization of MCF7 cells to the chemotherapeutic agent cis-diamminedichloroplatinum (II) (CDDP) by stabilizing p53. Interestingly, Ell3 induced p53 stabilization in response to CDDP by promoting binding of p53 to NADH quinoneoxidoreductase 1 (NQO1), which is linked to an ubiquitin-independent degradation pathway, as well as by suppressing a MDM2 mediated ubiquitin-dependent degradation pathway. Furthermore, Ell3 enhanced interleukin-20 (IL-20) expression leading to the activation of the ERK1/2 signaling pathway. By analyzing the suppressive effects of IL-20 and ERK signaling in the Ell3 expressing MCF7 cells, we confirmed that the IL-20 mediated ERK1/2 signaling pathway is the main cause of p53 stabilization after CDDP exposure in MCF7 cells. Ell3-overexpressing breast cancer cell lines were established using the chromosomal integration of an Ell3 expression plasmid, which was constructed by cloning PCR-amplified Ell3 cDNA into pcDNA3.1 vectors (Invitrogen, Carlsbad, CA; https://www.lifetechnologies.com). Three independent Ell3 overexpressing cell lines were generated. The gene expression profiles of wild type MCF7 and Ell3 overexpressing cell line were compared using Affymetrix PrimeView arrays.
2015-11-25 | E-GEOD-63612 | biostudies-arrayexpress
Project description:Human mesenchymal stem cell (MSC)-conditioned medium (CM) was previously reported to affect the biology of tumor cells; however, the precise mechanisms remain unclear. Here, we show that MSCs secreted 40- to 100-nm particles, which have the typical characteristics of exosomes, and these MSC-derived exosomes promoted migration of the breast cancer cell line MCF7. To further investigate the effect of MSC-exosomes on MCF7, we analyzed the gene expression profiles of MCF7 treated with or without MSC-exosomes for 24 h. Investigation of whole genome gene expression level changes in breast cancer cell line MCF7 which were treated with or without mesenchymal stem cell-derived exosomes. This study uses total RNA recovered from two samples. One sample is MCF7 treated with PBS for 24 hours and another one is MCF7 treated with mesenchymal stem cell-derived exosomes for 24hours. The ultimate concentration of mesenchymal stem cell-derived exosomes used in this experiment was 400ng/ul.
2013-05-20 | E-GEOD-46950 | biostudies-arrayexpress
Project description:The CCND1 gene, which is frequently overexpressed in cancers, encodes the regulatory subunit of a holoenzyme that phosphorylates the retinoblastoma protein (pRb). It is known that cyclin D1 regulates ERα transactivation using heterologous reporter systems, the significance of this observation to E2 dependent gene activation is unknow. E2 stimulated MCF7 cells treated with cyclin D1 siRNA in order to analyze the genes regulated by estradiol in a cyclin D1 dependent manner. Hormone deprived MCF7 cells were treated with cyclin D1 siRNA or control siRNA and stimulated with E2 or vehicle
2013-07-18 | GSE48989 | GEO
Project description:This study was amied to identify the diffenetiall expressed miRNAs in Withaferin A (WA) treated breast normal cells (MCF10A) in comparision to non-treated cells
2024-07-16 | GSE180247 | GEO
Project description:The CCND1 gene, which is frequently overexpressed in cancers, encodes the regulatory subunit of a holoenzyme that phosphorylates the retinoblastoma protein (pRb). It is known that cyclin D1 regulates ERM-NM-1 transactivation using heterologous reporter systems, the significance of this observation to E2 dependent gene activation is unknow. E2 stimulated MCF7 cells treated with cyclin D1 siRNA in order to analyze the genes regulated by estradiol in a cyclin D1 dependent manner. Hormone deprived MCF7 cells were treated with cyclin D1 siRNA or control siRNA and stimulated with E2 or vehicle Four separate 10cm plates of MCF7 cells treated with control siRNA were compared to four 10cm plates of MCF7 cells treated with cyclin D1 siRNA. 2 plates in each group treated with vehicle and two plates treated with E2.
2013-07-18 | E-GEOD-48989 | biostudies-arrayexpress
Project description:The effects of the CDK inhibitor PHA-848125 (referred to as CDK-125) on the MCF7 human adenocarcinoma mammary cell line were analysed by gene expression profiling. The MCF7 cell line was treated with PHA-848125 for 6 hours at a dose equal to 5 times the IC50. Untreated MCF7 cells were used as a control. Two replicates per treatment.
2010-07-14 | E-GEOD-18501 | biostudies-arrayexpress