Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA134091 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The forkhead transcription factor FOXM1 is a key regulator of the cell cycle and is overexpressed in cancer. Increased levels of FOXM1 are associated with both poor prognosis and oestrogen receptor (ERalpha) status in primary breast cancer. In this study, we map FOXM1 binding genome wide in both ERalpha-positive (MCF-7) and -negative (MDA-MB-231) breast cancer cells. We identify a common set of FOXM1 binding events at cell cycle-regulating genes, but in addition, in MCF-7 cells we find a high level of concordance with ERalpha-binding regions. FOXM1 binding at these co-binding sites is dependent on ERalpha binding, as depletion of ER protein levels reduced FOXM1 binding. FOXM1 interacts directly with both ERalpha co-activator CARM1 and is required for H3 arginine methylation at the ERalpha complex. Inhibition of FOXM1 activity with the ligand thiostrepton resulted in decreased FOXM1 binding at cca. 1400 sites genome wide and reduced expression of genes correlated with poor prognosis in ERalpha-positive tumour samples. These data demonstrate a novel role for the forkhead protein FOXM1 as an ERalpha cofactor and provide insight into the role of FOXM1 in ERalpha-positive breast cancer. The FOXM1-binding sites were mapped by ChIP-Seq in MCF-7 and MDA-MB-231 cells. Cells were treated either with thiostrepton, a FOXM1 inhibitor, or with DMSO (as control). Four replicates were performed in MCF7 cells and two replicates in MDA-MB-231 cells.
2013-01-07 | E-GEOD-40762 | biostudies-arrayexpress
Project description:Aurora Kinase B and ZAK interaction model
Equivalent of the stochastic model used in "Network pharmacology model predicts combined Aurora B and ZAK inhibition in MDA-MB-231 breast cancer cells" by Tang et. al. 2018.
The only difference is cell division and partitioning of the components, which are available in the original model for SGNS2.
2020-04-28 | BIOMD0000000940 | BioModels
Project description:Transcription factors (TFs) play a crucial role in diverse cellular physiology by controlling down-stream target genes. It has been well recognized that TFs are attractive target for treating human cancer since transcriptional activity or gene expression level of TFs can be directly modulated. To explore which TF functions as survival factor in human breast cancer, we applied gene expression data sets for survival analysis. We identified that FOXM1 is a potent oncogenic survival factor out of eleven TFs. Loss of FOXM1 function leads to breast cancer cells more sensitized to Doxorubicin (Dox). To investigate how FOXM1 sensitizes cancer cell in the presence of Dox, we carried out gene expression array experiment to monitor how down-stream target genes are changed by FOXM1. MDA-MB-231 cells were incubated with siLuc or siFOXM1. Thirty six hours later, cells were incubated with Dox (5micro mol) for 36 hrs. 3 siLuc., 3 siFOXM1, 3 siLuc and Dox treatment, 3 siFOXM1 and Dox treatment
2012-05-14 | E-GEOD-25741 | biostudies-arrayexpress
Project description:MDA-MB-231 breast cancer cells were treated with docosahexaenoic acid with or without doxorubicin chemotherapy Microarrays were used to detail changes in gene expression in the treatments
2018-04-21 | GSE113427 | GEO
Project description:Imipramine Blue a novel inhibitor that we recently synthesiszed suppressed breast cancer growth and progression by silencing FOXM1 and its associated signaling. Breast cancer cell-line MDA-MB-231 treated with vehicle (DMSO) and IB, with 2 biological replciates each.
2016-08-10 | E-GEOD-72363 | biostudies-arrayexpress
Project description:Transcription factors (TFs) play a crucial role in diverse cellular physiology by controlling down-stream target genes. It has been well recognized that TFs are attractive target for treating human cancer since transcriptional activity or gene expression level of TFs can be directly modulated. To explore which TF functions as survival factor in human breast cancer, we applied gene expression data sets for survival analysis. We identified that FOXM1 is a potent oncogenic survival factor out of eleven TFs. Loss of FOXM1 function leads to breast cancer cells more sensitized to Doxorubicin (Dox). To investigate how FOXM1 sensitizes cancer cell in the presence of Dox, we carried out gene expression array experiment to monitor how down-stream target genes are changed by FOXM1. MDA-MB-231 cells were incubated with siLuc or siFOXM1. Thirty six hours later, cells were incubated with Dox (5micro mol) for 36 hrs.
2012-05-15 | GSE25741 | GEO
Project description:NF-kB has been linked to doxorubicin-based chemotherapy resistance in breast cancer patients. NF-kB nuclear translocation and DNA binding in doxorubicin treated-breast cancer cells have been extensively examined, however its functional consequences in terms the spectrum of NF-kB -dependent genes expressed and, thus, the impact on tumour cell behaviour are unclear. We hypothesized that NF-kB gene expression profile induced by doxorubicin might be different among breast cancer cells and tumors. Doxorubicin treatment in the p53-mutated MDA-MB-231 cells resulted in NF-kB driven-gene transcription demonstrated by gene expression microarrays. Selected genes (ICAM-1, CXCL1, IL8) related with invasion, metastasis and chemoresistance expression were confirmed by RT-PCR in a subset of additional doxorubicin-treated cells and fresh primary human breast tumors. In both systems, p53-deficient background correlated with the activation of these NF-kB targeted genes. Overexpression of p53WT in the mutant p53 MDA-MB-231 cells impaired NF-kB driven transcription induced by doxorubicin. Moreover, tumors with a p53 deficient background and nuclear NF-kB /p65 expression correlated with reduced disease free-survival. This study supports that tumor molecular profiles for doxorubicin driven NF-kB-response are likely to exist. A link between p53 deficiency and the presence of active transcriptionally NF-kB could favour an aggressive behaviour and might have implications for doxorubicin-based chemotherapy in breast tumors exhibiting aberrant p53 activity 12 samples were analyzed: controls (n=3); Doxorubicin treated (n=3); MLN120B treated (n=3); MLN120B + Doxorubicin treated (n=3)
2013-12-31 | E-GEOD-47013 | biostudies-arrayexpress
Project description:Human breast cancer MDA-MB-231 cell siControl and siICAM1
2021-05-25 | PXD026234 | JPOST Repository
Project description:MDA-MB-231 breast cancer cells and MCF-10A breast cells were exposed to 1 mT 50 Hz extremely low-frequency magnetic field (ELF-MF) for 4 hours
2023-02-17 | PXD040120 | JPOST Repository
Project description:NF-kB has been linked to doxorubicin-based chemotherapy resistance in breast cancer patients. NF-kB nuclear translocation and DNA binding in doxorubicin treated-breast cancer cells have been extensively examined, however its functional consequences in terms the spectrum of NF-kB -dependent genes expressed and, thus, the impact on tumour cell behaviour are unclear. We hypothesized that NF-kB gene expression profile induced by doxorubicin might be different among breast cancer cells and tumors. Doxorubicin treatment in the p53-mutated MDA-MB-231 cells resulted in NF-kB driven-gene transcription demonstrated by gene expression microarrays. Selected genes (ICAM-1, CXCL1, IL8) related with invasion, metastasis and chemoresistance expression were confirmed by RT-PCR in a subset of additional doxorubicin-treated cells and fresh primary human breast tumors. In both systems, p53-deficient background correlated with the activation of these NF-kB targeted genes. Overexpression of p53WT in the mutant p53 MDA-MB-231 cells impaired NF-kB driven transcription induced by doxorubicin. Moreover, tumors with a p53 deficient background and nuclear NF-kB /p65 expression correlated with reduced disease free-survival. This study supports that tumor molecular profiles for doxorubicin driven NF-kB-response are likely to exist. A link between p53 deficiency and the presence of active transcriptionally NF-kB could favour an aggressive behaviour and might have implications for doxorubicin-based chemotherapy in breast tumors exhibiting aberrant p53 activity
2013-12-31 | GSE47013 | GEO