Project description:The study aimed at finding the molecular mechanism of action of PL and AP in breast cancer cells. The dataset shows the comparison of gene expression in Plumbagin/Acetyl Plymbagin treated MCF-7 cells when compared with untreated samples.
Project description:The study aimed at finding the molecular mechanism of action of PL and AP in breast cancer cells. The dataset shows the comparison of gene expression in Plumbagin/Acetyl Plymbagin treated MCF-7 cells when compared with untreated samples. 11 samples were analyzed. MCF-7 cells treated with 10 uM PL or AP for 6 hours. Please note that three samples were done in triplicates and one sample MCF-7 treated with 10uM PL was done in duplicates as one of the replicate RNA didn't show up a good RIN number, SAMPLE1 &2 are replicates, SAMPLE 3,4 &5 are triplicates, SAMPLE 6,7 & 8 are triplicates and SAMPLE 9,10 & 11 are triplicates (SAMPLE numbers are indicated in the description field).
Project description:E. coli MG1655 was grown in the presence of either PL (Plumbagin)/JU (Juglone)/ME (Menadione) (50 micro molar) and DMSO (0.75%)as control, and subjected to microarray analysis. The aim of the work was to understand the structure-function relationship between plumbagin and its analogues.
Project description:This work investigated the molecular mechanisms unterlying the previously reported anticancer activity of the usnic acid isoxazole derivative, named 2b. Using RNA-seq technology transcriptoms of MCF-7 breast cancer cells treated with vehicle or 2b for two diffrent time periods were compared. Among differentially expressed genes, components of the protein processing in endoplasmic reticulum pathway were the most significantly upregulated by 2b.
Project description:We provide label-free data-dependent acquisition proteomics data of mcf-7 breast cancer cell lines treated with the pure minor hop compounds xanthohumol and xanthohumol c.
Project description:Transcriptional profiling of human MCF-7 breast cancer cells comparing MCF-7 cells treated with control medium (DMEM/F12 + 0,5% BSA) with MCF-7 cells treated with conditioned medium of cancer-associated adipose tissue (CMCAAT) obtained from 2 breast cancer patients. Goal was to determine the effects of CMCAAT treatment on global MCF-7 gene expression.
Project description:Sharing common ErbB/HER receptor signaling pathway, heregulin (HRG) induces differentiation of MCF-7 breast cancer cells while epidermal growth factor (EGF) elicits proliferation. Although the cell fate led by those two ligands was totally different, the gene expression profile in early transcription was unexpectedly qualitatively similar, suggesting that the gene expression in late transcription, not early transcription, may reflect a respect of ligand specificity. In this study, based on the data from time-course microarray of all human genes, we predicted and determined a series of transcription factors which may control HRG-specific timed-late transcription and cellular differentiation of MCF-7 cells. Validation analyses showed that one of activator protein 1 (AP-1) families appeared just after c-Fos expression, another AP-1 family partner, induced expression of another transcription factor through activation of AP-1 complex. Furthermore, expression of this transcription factors caused suppression of extracellular signal-regulated kinase (ERK) phosphorylation which is sustainedly regulated by HRG-initiated ErbB signaling. Overall, our analysis indicated an importance of formation of timed-transcriptional regulatory network and its function to control upstream signaling pathway through negative feedback for cellular differentiation. Experiment Overall Design: MCF7 human breast cancer cells were stimulated by the growth hormone (epidermal growth factor (EGF) or heregulin (HRG)). Control was set as non-treated cells.
Project description:Overexpression of the AP-2γ transcription factor in breast tumours has been identified as an independent predictor of poor outcome and failure of hormone therapy, even in ER positive, ErbB2 negative tumours; markers of a more favourable prognosis. To understand further the role of AP-2γ in breast carcinoma, we have used an RNA interference and gene expression profiling strategy using the MCF-7 cell line as a model for ER positive, ErbB2 negative tumours with AP-2γ overexpression. Gene expression changes between control and silenced cells implicate AP-2γ in the control of cell cycle progression and developmental signalling. Experiment Overall Design: We compared the expression profiles of MCF-7 cells separately transfected with three independent AP-2γ targeting sequences with those from control cells treated with transfection reagent alone or a non-silencing control siRNA on Affymetrix arrays; each condition was examined in triplicate.
Project description:Estrogen receptor alpha (ERalpha) is a ligand-dependent transcription factor that plays an important role in breast cancer. Estrogen-dependent gene regulation by ERalpha can be mediated by interaction with other DNA-binding proteins, such as activator protein-1 (AP-1). The nature of such interactions in mediating the estrogen response in breast cancer cells remains unclear. Here we show that knockdown of c-Fos, a component of the transcription factor AP-1, attenuates the expression of 37% of all estrogen-regulated genes, suggesting that AP-1 is a fundamental factor for ERalpha-mediated transcription. Additionally, knockdown of c-Fos affected the expression of a number of genes that were not regulated by estrogen. Pathway analysis reveals that silencing of c-Fos downregulates an E2F1-dependent pro-proliferative gene network. Thus, modulation of the E2F1 pathway by c-Fos represents a novel mechanism by which c-Fos enhances breast cancer cell proliferation. Furthermore, we show that c-Fos and ERalpha can cooperate in regulating E2F1 gene expression by binding to regulatory elements in the E2F1 promoter. To start to dissect the molecular details of the cross-talk between AP-1 and estrogen signaling, we identify a novel ERalpha/AP-1 target, PKIB (cAMP-dependent protein kinase inhibitor-beta), which is overexpressed in ERalpha-positive breast cancer tissues. Knockdown of PKIB by siRNA results in drastic growth suppression of breast cancer cells. Collectively, our findings support AP-1 as a critical factor that governs estrogen-dependent gene expression and breast cancer proliferation programs. MCF-7 cells were transfected with a control siRNA or with the pool of siRNAs targeting c-Fos for 72 h and were then treated with vehicle or E2 for 24 h, and global gene expression profiles were assessed. Three or four biological replicates were used for each group.
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.