Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA147639 | ENA |
REPOSITORIES: ENA
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Project description:Na+/I- symporter (NIS)-mediated iodide uptake allows radioiodine therapy for thyroid cancer. NIS is also expressed in breast tumors, raising potential for radionuclide therapy of breast cancer. However, NIS expression in most breast cancers is low and may not be sufficient for radionuclide therapy. A better understanding of the mechanisms of NIS regulation in breast cancer may lead to strategies for increasing cell surface NIS and radioactive iodide uptake (RAIU) in breast cancer. The MCF-7 cell line is the only human breast cancer cell line with inducible endogenous NIS expression. Kogai et al. [2000] first reported that trans-retinoic acid (tRA) induces NIS mRNA expression in MCF-7 cells and it was later reported that a combination treatment of tRA and hydrocortisone (tRA/H) further increases tRA-induced NIS expression/function in MCF-7 cells (Kogai et al., 2005; Dohan et al., 2006). In this study, we used gene expression profiling to identify genes that correlate with NIS expression in MCF-7 cells such that mechanisms underlying NIS modulation may be elucidated.
2011-09-16 | GSE32161 | GEO
Project description:Na+/I- symporter (NIS)-mediated iodide uptake allows radioiodine therapy for thyroid cancer. NIS is also expressed in breast tumors, raising potential for radionuclide therapy of breast cancer. However, NIS expression in most breast cancers is low and may not be sufficient for radionuclide therapy. A better understanding of the mechanisms of NIS regulation in breast cancer may lead to strategies for increasing cell surface NIS and radioactive iodide uptake (RAIU) in breast cancer. The MCF-7 cell line is the only human breast cancer cell line with inducible endogenous NIS expression. Kogai et al. [2000] first reported that trans-retinoic acid (tRA) induces NIS mRNA expression in MCF-7 cells and it was later reported that a combination treatment of tRA and hydrocortisone (tRA/H) further increases tRA-induced NIS expression/function in MCF-7 cells (Kogai et al., 2005; Dohan et al., 2006). In this study, we used gene expression profiling to identify genes that correlate with NIS expression in MCF-7 cells such that mechanisms underlying NIS modulation may be elucidated. MCF-7 cells were treated with DMSO vehicle, tRA (1µM), or tRA(1µM)/H(1µM) for 12 hours and total RNA was extracted. There are two replicates for each treatment group.
2011-09-15 | E-GEOD-32161 | biostudies-arrayexpress
Project description:We performed a microarray analysis to compare the expression profile of azurin treated and untreated with different P-cadherin expression levels. We also compared the differentially expressed genes regulated by P-cadherin overexpression. Both cell lines presented an up-regulation of apoptosis mediated by p53 protein, endocytosis and vesicle-mediated transport. Conversely, invasive MCF-7/AZ.Pcad cells treated with azurin presented a decreased expression of genes associated with cell surface receptors and signal transduction, as well as genes associated with biological adhesion and migration. Azurin is a bacterial protein from Pseudomonas aeruginosa which exerts an inhibitory activity in cancer cells. In P-cadherin-overexpressing models, a bad prognosis marker in breast cancer increasing invasion and other malignant features, azurin decreases the invasion of cancer cells. We performed a microarray analysis to compare the expression profile of azurin treated cells with different P-cadherin expression levels. Azurin up-regulated apoptosis mediated by p53 protein, endocytosis and vesicle-mediated transport. In the contrary, in invasive MCF-7/AZ.Pcad cells, azurin decreased the expression of genes associated with cell surface receptors and signal transduction, as well as biological adhesion. Further, azurin decreased adhesion of cells to proteins from the Extracellular matrix (ECM) and altered protein expression of integrins α6, β4 and β1 and interfered with the ability of these cells to form mammospheres. Altogether, our results further enlighten the anti-cancer effects mediated by azurin in P-cadherin overexpression breast cancer models.
2014-04-30 | GSE54319 | GEO
Project description:We performed a microarray analysis to compare the expression profile of azurin treated and untreated with different P-cadherin expression levels. We also compared the differentially expressed genes regulated by P-cadherin overexpression. Both cell lines presented an up-regulation of apoptosis mediated by p53 protein, endocytosis and vesicle-mediated transport. Conversely, invasive MCF-7/AZ.Pcad cells treated with azurin presented a decreased expression of genes associated with cell surface receptors and signal transduction, as well as genes associated with biological adhesion and migration. Azurin is a bacterial protein from Pseudomonas aeruginosa which exerts an inhibitory activity in cancer cells. In P-cadherin-overexpressing models, a bad prognosis marker in breast cancer increasing invasion and other malignant features, azurin decreases the invasion of cancer cells. We performed a microarray analysis to compare the expression profile of azurin treated cells with different P-cadherin expression levels. Azurin up-regulated apoptosis mediated by p53 protein, endocytosis and vesicle-mediated transport. In the contrary, in invasive MCF-7/AZ.Pcad cells, azurin decreased the expression of genes associated with cell surface receptors and signal transduction, as well as biological adhesion. Further, azurin decreased adhesion of cells to proteins from the Extracellular matrix (ECM) and altered protein expression of integrins M-NM-16, M-NM-24 and M-NM-21 and interfered with the ability of these cells to form mammospheres. Altogether, our results further enlighten the anti-cancer effects mediated by azurin in P-cadherin overexpression breast cancer models. Cells were exposed to azurin (100uM) for 48h, after which total RNA was extracted. Control cells were exposed during the same time to PBS buffer solution. Three independent samples for each condition were used treated with different azurin production batches.
2014-04-30 | E-GEOD-54319 | biostudies-arrayexpress
Project description:In the normal breast, PMCA2 transports calcium into milk. It is also upregulated in breast cancer cells and high tumor levels predict increased mortality in patients. In this study, we examined interactions between PMCA2 and HER2. We find that PMCA2 and a scaffolding protein, NHERF1, interact together with HER2 in specific membrane domains protruding from the surface of breast cancer cells. Knocking down PMCA2 or NHERF1 increases intracellular calcium and leads to the ubiquitination, endocytosis and degradation of HER2 after receptor activation. This is associated with reductions in HER2 expression and signaling. Manipulating PMCA2 levels regulates proliferation and apoptosis of breast cancer cells in vitro and knocking out PMCA2 dramatically inhibits the formation of hyperplasia and tumors in MMTV-Neu mice. Gene expression profiling was performed on control SKBR3 cells vs. PMCA2, NHERFR1 and HER2 knock down cells. Each group has 6 duplicates.
2014-10-22 | E-GEOD-62555 | biostudies-arrayexpress
Project description:By coupling PDX and cell surface marker screening technologies, we have identified distinct tumor cell sub-populations that are associated with tumor resistance to chemotherapy. In the majority of relapsed tumors, the percentage of the marker-positive cells shifted back to pretreatment levels. SSEA4 is one of the cell surface molecules tested that could distinguish enriched residual tumor cells in all the different TNBC PDX models analyzed. The expression of SSEA4 is associated with tumor resistance to chemotherapy and SSEA4+ cells show increased gene expression of genes involved in response to toxins, cellular import/export, cell migration and EMT. The dataset comprises four different sample groups including SSEA4- and SSEA4+ cell fractions isolated from mouse xenografts of human breast cancer cells. Two technical replicates were generated for each cell fraction. Microarray analysis was performed on the Agilent Whole Human Genome Oligo Microarray 8x60K (v2) platform.
2015-11-19 | E-GEOD-57704 | biostudies-arrayexpress
Project description:By coupling PDX and cell surface marker screening technologies, we have identified distinct tumor cell sub-populations that are associated with tumor resistance to chemotherapy. In the majority of relapsed tumors, the percentage of the marker-positive cells shifted back to pretreatment levels. SSEA4 is one of the cell surface molecules tested that could distinguish enriched residual tumor cells in all the different TNBC PDX models analyzed. The expression of SSEA4 is associated with tumor resistance to chemotherapy and SSEA4+ cells show increased gene expression of genes involved in response to toxins, cellular import/export, cell migration and EMT. The dataset comprises four different sample groups including SSEA4- and SSEA4+ cell fractions isolated from mouse xenografts of human breast cancer cells. Two technical replicates were generated for each cell fraction. Microarray analysis was performed on the Agilent Whole Human Genome Oligo Microarray 8x60K (v2) platform.
2015-11-19 | E-GEOD-57703 | biostudies-arrayexpress
Project description:In the normal breast, PMCA2 transports calcium into milk. It is also upregulated in breast cancer cells and high tumor levels predict increased mortality in patients. In this study, we examined interactions between PMCA2 and HER2. We find that PMCA2 and a scaffolding protein, NHERF1, interact together with HER2 in specific membrane domains protruding from the surface of breast cancer cells. Knocking down PMCA2 or NHERF1 increases intracellular calcium and leads to the ubiquitination, endocytosis and degradation of HER2 after receptor activation. This is associated with reductions in HER2 expression and signaling. Manipulating PMCA2 levels regulates proliferation and apoptosis of breast cancer cells in vitro and knocking out PMCA2 dramatically inhibits the formation of hyperplasia and tumors in MMTV-Neu mice.
2014-10-22 | GSE62555 | GEO
Project description:This study introduces a predictive classifier for breast cancer-related proteins, utilising a combination of protein sequence descriptors and machine learning techniques. The best-performing classifier is a Multi Layer Perceptron (artificial neural network) with 300 features, achieving an average Area Under the Receiver Operating Characteristics (AUROC) score of 0.984 through 3-fold cross-validation. Notably, the model identified top-ranked cancer immunotherapy proteins associated with breast cancer that should be studied for further biomarker discovery and therapeutic targeting.
Please note that in this model, the output '0' means BC non-related protein and '1' means BC related protein. The original GitHub repository can be accessed at https://github.com/muntisa/neural-networks-for-breast-cancer-proteins
2023-10-09 | BIOMD0000001076 | BioModels
Project description:Analysis of RNA immunoprecipitation of HuR, a RNA binding protein (RBP), in breast cancer cell lines. This approach, utilizing RNA immunoprecipitation hybridized to microarray (RIP-Chip), provides global identification of putative endogenous mRNA targets of different RBPs. HuR is an RBP that binds to the AU-rich (ARE) regions of labile mRNAs, such as proto-oncogenes, facilitating their translation into protein. HuR has been shown to play a role in cancer progression and elevated levels of cytoplasmic HuR directly correlate with increased invasiveness and poor prognosis for many cancers, including those of the breast. We used HuR RIP-Chip as a comprehensive and systematic method to survey breast cancer target genes in both MCF-7 (estrogen receptor positive, ER+) and MDA-MB-231 (estrogen receptor negative, ER-) breast cancer cell lines. We identified unique subsets of HuR associated mRNAs found individually or in both cell types. Two novel HuR targets, CD-9 and CALM-2, were identified and validated by quantitative RT-PCR and biotin pulldown analysis. Our findings reveal that the differential regulation of these two cancer-related genes by HuR was contingent upon the cellular environment. RNA immunoprecipitation of the HuR RNA binding protein by 3A2 antibody and IgG (control) from two human breast cancer cell lines, MCF-7 and MDA-MB-231 .
2010-06-24 | E-GEOD-17820 | biostudies-arrayexpress