Exon arrays from HT-29, MCF10A, and MDA-MB-436 cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Kang Byong
PROVIDER: S-ECPF-GEOD-45195 | biostudies-other |
REPOSITORIES: biostudies-other
Similar Datasets
Project description:Expression data from HT-29 cells treated with IFN-γ for 24 hr, MCF10A cells, and MDA-MB-436 cells.
2013-08-06 | GSE45195 | GEO
Project description:Expression data from HT-29 cells treated with IFN-γ for 24 hr, MCF10A cells, and MDA-MB-436 cells. Total RNA was isolated with the RNeasy Mini Kit (Qiagen). Sense-strand cDNA synthesis, terminal labeling, and hybridization were performed using Ambion WT Expression Kit (Applied Biosystems, P/N 4425209).
2013-08-06 | E-GEOD-45195 | biostudies-arrayexpress
Project description:RNA-seq data from HT-29 cells treated with IFN-γ for 24 hr, MCF10A cells, and MDA-MB-436 cells. mRNA profiles of HT-29, MCF10A, and MDA-MB-436 were generated by deep sequencing using Illumina HiSeq 2000. All RNA sequencing data was generated by the Genomics Services Lab at the HudsonAlpha Institute for Biotechnology (Huntsville, AL).
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Project description:RNA-seq data from HT-29 cells treated with IFN-γ for 24 hr, MCF10A cells, and MDA-MB-436 cells.
2013-08-06 | GSE45258 | GEO
Project description:RNA-seq data from HT-29 cells treated with IFN-M-NM-3 for 24 hr, MCF10A cells, and MDA-MB-436 cells. mRNA profiles of HT-29, MCF10A, and MDA-MB-436 were generated by deep sequencing using Illumina HiSeq 2000. All RNA sequencing data was generated by the Genomics Services Lab at the HudsonAlpha Institute for Biotechnology (Huntsville, AL).
2013-08-06 | E-GEOD-45258 | biostudies-arrayexpress
Project description:Metastasis remains a major clinical problem in cancer diagnosis and treatment. Metastasis is the leading cause of cancer‑related mortality but is still poorly understood. Cytoskeletal proteins are considered potential therapeutic targets for metastatic cancer cells because the cytoskeleton serves a key role in the migration and invasion of these cells. Vimentin and F‑actin exhibit several functional similarities and undergo quantitative and structural changes during carcinogenesis. The present study investigated the effects of vimentin and F‑actin deficiency on the survival and motility of breast cancer cells. In metastatic breast cancer cells (MDA‑MB‑231) and breast epithelial cells (MCF10A), vimentin was knocked down by small interfering RNA and F‑actin was depolymerized by latrunculin A, respectively. The effect of reduced vimentin and F‑actin content on cell viability was analyzed using the MTT assay and the proliferative capacity was compared by analyzing the recovery rate. The effect on motility was analyzed based on two processes: The distance traveled by tracking the cell nucleus and the movement of the protrusions. The effects on cell elasticity were measured using atomic force microscopy. Separately reducing vimentin or F‑actin did not effectively inhibit the growth and motility of MDA‑MB‑231 cells; however, when both vimentin and F‑actin were simultaneously deficient, MDA‑MB‑231 cells growth and migration were severely impaired. Vimentin deficiency in MDA‑MB‑231 cells was compensated by an increase in F‑actin polymerization, but no complementary action of vimentin on the decrease in F‑actin was observed. In MCF10A cells, no complementary interaction was observed for both vimentin and F‑actin.
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Project description:In breast cancer cells, the linoleic acid (LA), an ω-6 essential polyunsaturated fatty acid, induces a variety of biological processes, including migration and invasion. Extracellular vesicles (EVs) are structures released by normal and malignant cells into extracellular space, and their function is dependent on their cargo and the cell type from which are secreted. Particularly, the EVs from MDA-MB-231 breast cancer cells treated with LA promote an epithelial-mesenchymal-transition (EMT)-like process in mammary non-tumorigenic epithelial cells MCF10A. Here, we found that EVs isolated from supernatants of MDA-MB-231 breast cancer cells stimulated with 90 μM LA induces activation of Akt2, FAK and ERK1/2 in MCF10A cells. In addition, EVs induces migration through a PI3K, Akt and ERK1/2-dependent pathway, whereas invasion is dependent on PI3K activity.
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Project description:To determine the effect ALDH1A3 expression on global gene expression in MDA-MB-231 cells and MDA-MB-468 cells In MDA-MB-231 cells, ALDH1A3 was overexperssed (have low endogenous levels of ALDH1A3) and compared to MSCV empty vector control. In MDA-MB-468 cells that have high endogenous levels of ALDH1A3, ALDH1A3 expresion was reduced with ALDH1A3 shRNA1 and compared to scramble shRNA control.
| S-ECPF-GEOD-49322 | biostudies-other
Project description:Breast cancer remains a leading cause of death in women worldwide. Although breast cancer therapies have greatly advanced in recent years, many patients still develop tumour recurrence and metastasis, and eventually succumb to the disease due to chemoresistance. Citral has been reported to show cytotoxic effect on various cancer cell lines. However, the potential of citral to specifically target the drug resistant breast cancer cells has not yet been tested, which was the focus of our current study.The cytotoxic activity of citral was first tested on MDA-MB-231 cells in vitro by MTT assay. Subsequently, spheroids of MDA-MB-231 breast cancer cells were developed and treated with citral at different concentrations. Doxorubicin, cisplatin and tamoxifen were used as positive controls to evaluate the drug resistance phenotype of MDA-MB-231 spheroids. In addition, apoptosis study was performed using AnnexinV/7AAD flowcytometry. Aldefluor assay was also carried out to examine whether citral could inhibit the ALDH-positive population, while the potential mechanism of the effect of citral was carried out by using quantitative real time- PCR followed by western blotting analysis.Citral was able to inhibit the growth of the MDA-MB-231 spheroids when compared to a monolayer culture of MDA-MB-231 cells at a lower IC50 value. To confirm the inhibition of spheroid self-renewal capacity, the primary spheroids were then cultured to additional passages in the absence of citral. A significant reduction in the number of secondary spheroids were formed, suggesting the reduction of self-renewal capacity of these aldehyde dehydrogenase positive (ALDH+) drug resistant spheroids. Moreover, the AnnexinV/7AAD results demonstrated that citral induced both early and late apoptotic changes in a dose-dependent manner compared to the vehicle control. Furthermore, citral treated spheroids showed lower cell renewal capacity compared to the vehicle control spheroids in the mammosphere formation assay. Gene expression studies using quantitative real time PCR and Western blotting assays showed that citral was able to suppress the self-renewal capacity of spheroids and downregulate the Wnt/?-catenin pathway.The results suggest that citral could be a potential new agent which can eliminate drug-resistant breast cancer cells in a spheroid model via inducing apoptosis.
| S-EPMC5809808 | biostudies-literature
Project description:Since bone metastatic breast cancer is an incurable disease, causing significant morbidity and mortality, understanding of the underlying molecular mechanisms would be highly valuable. Here, we describe in vitro and in vivo evidence for the importance of serine biosynthesis in the metastasis of breast cancer to bone. We first characterized the bone metastatic propensity of the MDA-MB-231(SA) cell line variant as compared to the parental MDA-MB-231 cells by radiographic and histological observations in the inoculated mice. Genome-wide gene expression profiling of this isogenic cell line pair revealed that all the three genes involved in the L-serine biosynthesis pathway, phosphoglycerate dehydrogenase (PHGDH), phosphoserine aminotransferase 1 (PSAT1), and phosphoserine phosphatase (PSPH) were upregulated in the highly metastatic variant. This pathway is the primary endogenous source for L-serine in mammalian tissues. Consistently, we observed that the proliferation of MDA-MB-231(SA) cells in serine-free conditions was dependent on PSAT1 expression. In addition, we observed that L-serine is essential for the formation of bone resorbing human osteoclasts and may thus contribute to the vicious cycle of osteolytic bone metastasis. High expression of PHGDH and PSAT1 in primary breast cancer was significantly associated with decreased relapse-free and overall survival of patients and malignant phenotypic features of breast cancer. In conclusion, high expression of serine biosynthesis genes in metastatic breast cancer cells and the stimulating effect of L-serine on osteoclastogenesis and cancer cell proliferation indicate a functionally critical role for serine biosynthesis in bone metastatic breast cancer and thereby an opportunity for targeted therapeutic interventions. Parental MDA-MB-231 cells and MDA-MB-231(SA) cells were cultured in cell culture flasks. RNA was isolated in order to compare the gene expression profiles of these cell variants. Total of two samples. No replicates.
| S-ECPF-GEOD-20085 | biostudies-other