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Gene expression profile of FOXM1 with Doxorubicin in MDA-MB-231 breast cancer cells

ABSTRACT: 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

ORGANISM(S): Homo sapiens

SUBMITTER: Park YY

PROVIDER: S-ECPF-GEOD-25741 | biostudies-other | 2012 Oct

REPOSITORIES: biostudies-other

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Gene expression profile of FOXM1 with Doxorubicin in MDA-MB-231 breast cancer cells

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

Gene expression profile of FOXM1 with Doxorubicin in MDA-MB-231 breast cancer cells

2012-05-14 | E-GEOD-25741 | biostudies-arrayexpress

Integrin ?3b1-dependent gene expression in MDA-MB-231 breast cancer cells

Project description:Gene-level and exon-level analysis of gene expression in MDA-MB-231 cells that stably express control shRNA or integrin α3-targeting shRNA. The laminin-332-binding integrin α3b1 is expressed highly in many breast cancer cells, but its roles in regulating gene expression programs that promote breast cancer progression have not been explored. In order to identify genes that are regulated by α3b1 in human breast cancer cells, we used a lentiviral approach to express an α3-targeting shRNA to suppress integrin α3b1 in MDA-MB-231 cells, and we identified subsequent changes in gene expression and alternate exon useage. We used the Affymetrix Human Exon 1.0 ST platform to analyze biological replicates of MDA-MB-231 cells that were transduced with lentivirus to stably express either control shRNA or α3-targeting shRNA. Array data was processed by Affymetrix Exon Array Computational Tool.

| S-ECPF-GEOD-43097 | biostudies-other

Extracellular Matrix Components Regulate Bone Sialoprotein Expression in MDA-MB-231 Breast Cancer Cells.

Project description:Bone sialoprotein (BSP) has become a target in breast cancer research as it is associated with tumor progression and metastasis. The mechanisms underlying the regulation of BSP expression have been largely elusive. Given that BSP is involved in the homing of cancer cells in bone metastatic niches, we addressed regulatory effects of proteolytic cleavage and extracellular matrix components on BSP expression and distribution in cell culture models. Therefore, MDA-MB-231 human breast cancer cells were kept in 2D and 3D spheroid cultures and exposed to basement membrane extract in the presence or absence of matrix metalloproteinase 9 or the non-polar protease, dispase. Confocal imaging of immunofluorescence samples stained with different antibodies against human BSP demonstrated a strong inducing effect of basement membrane extract on anti-BSP immunofluorescence. Similarly, protease incubation led to acute upregulation of anti-BSP immunofluorescence signals, which was blocked by cycloheximide, suggesting de novo formation of BSP. In summary, our data show that extracellular matrix components play an important function in regulating BSP expression and hint at mechanisms for the formation of bone-associated metastasis in breast cancer that might involve local control of BSP levels by extracellular matrix degradation and release of growth factors.

| S-EPMC8225072 | biostudies-literature

Elastin molecular aging promotes MDA-MB-231 breast cancer cell invasiveness.

Project description:Elastin is a long-lived extracellular matrix protein responsible for the structural integrity and function of tissues. Breast cancer elastosis is a complex phenomenon resulting in both the deposition of elastotic masses and the local production of elastin fragments. In invasive human breast cancers, an increase in elastosis is correlated with severity of the disease and age of the patient. Elastin-derived peptides (EDPs) are a hallmark of aging and are matrikines - matrix fragments having the ability to regulate cell physiology. They are known to promote processes linked to tumor progression, but their effects on breast cancer cells remain unexplored. Our data show that EDPs enhance the invasiveness of MDA-MB-231 breast cancer cells through the engagement of matrix metalloproteases 14 and 2. We therefore suggest that elastosis and/or an aged stroma could promote breast cancer cell invasiveness.

| S-EPMC6120250 | biostudies-literature

Effects of FSTL1 on cell proliferation in breast cancer cell line MDA‑MB‑231 and its brain metastatic variant MDA‑MB‑231‑BR.

Project description:In the past decades, altered Follistatin‑like 1 (FSTL1) expression has been documented in a variety of cancers, while its functional roles are poorly understood. Particularly in breast cancer, the expression of FSTL1 and its signaling pathway remain to be determined. In the present study, an elevated FSTL1 expression and a supressed cell proliferation were detected in a specific brain metastatic cell line MDA‑MB‑231‑BR (231‑BR), compared with its parental cell line MDA‑MB‑231. However, this protein was hardly detected in the other three breast cancer cell lines. Next, lentiviral vectors encoding FSTL1 or FSTL1 specific shRNAs were used to overexpress or knock down FSTL1 in MDA‑MB‑231 or 231‑BR, respectively (MDA‑MB‑231FSTL1 or 231‑BRsh FSTL1). Results showed that overexpression of FSTL1 inhibited MDA‑MB‑231 cell proliferation, while knockdown of FSTL1 in 231‑BR cells promotes cell proliferation, compared with their corresponding control groups. These results were further confirmed in nude mouse xenografts. The tumor volume in 231‑BR cell-bearing mice was significantly smaller than that of MDA‑MB‑231 group, and reduction of tumor volume was detected in MDA‑MB‑231FSTL1 cell-bearing mice compared with the control group. Previous studies revealed that TGF‑β-Smad2/3 signaling pathway was activated in 231‑BR and MDA‑MB‑231FSTL1 cells, which may contribute to the inhibited cell proliferation. In addition, Smad3 knockdown could restore the inhibition of cell proliferation induced by FSTL1 overexpression in MDA‑MB‑231FSTL1 cells, indicating that the anti‑proliferative effect of FSTL1 overexpression may be associated with Smad3 involved TGF‑β signaling pathway regulation. This study identified FSTL1 as an inhibitor of cell proliferation in MDA‑MB‑231 and 231‑BR cell lines, which may provide new insights into the development and management of breast cancer.

| S-EPMC5780039 | biostudies-literature

Amikacin Suppresses Human Breast Cancer Cell MDA-MB-231 Migration and Invasion.

Project description:(1) Background: Amikacin is an aminoglycoside antibiotic used for treating gram-negative bacterial infections in cancer patients. In this study, our aims are to investigate the migratory inhibition effects of amikacin in human MDA-MB-231 cells. (2) Methods: We used a wound-healing assay, trans-well analysis, Western blotting, immunostaining and siRNA knockdown approaches to investigate how amikacin influenced MDA-MB-231 cell migration and invasion. (3) Results: Wound healing showed that the MDA-MB-231 cell migration rates decreased to 44.4% in the presence of amikacin. Trans-well analysis showed that amikacin treatment led to invasion inhibition. Western blotting demonstrated that amikacin induced thioredoxin-interacting protein (TXNIP) up-regulation. TXNIP was knocked down using siRNA in MDA-MB-231 cell. Using immunostaining analysis, we found that inhibition of TXNIP expression led to MDA-MB-231 pseudopodia extension; however, amikacin treatment attenuated the cell extension formation. (4) Conclusions: We observed inhibition of migration and invasion in MDA-MB-231 cells treated with amikacin. This suggests inhibition might be mediated by up-regulation of TXNIP.

| S-EPMC7712503 | biostudies-literature

Glyco-gene expression in human breast cancer MDA-MB-231 cells treated with ManNAc analogs

Project description:Analogs of ManNAc, the committed precursor of sialic acid, decrease metastatic potential and trigger apoptosis in cancer cells. Adding Lev to ManNAc analogs increases their toxicity due to an ill-understood mechanism. Comparing gene expression profiles of cells treated with Ac4ManNLev and Ac4ManNAc will provide insight into the similarities and differences of these analogs. Specifically, MDA-MB-231 human breast cancer cells will be treated with Ac4ManNLev and Ac4ManNAc at doses that inhibit cell growth and induce the cell to undergo apoptosis later. RNA will be harvested in the early stage of cell arrest in order to identify genes altered by Ac4ManNLev and Ac4ManNAc. RNA preparations from three conditions, were sent to Microarray Core (E). One as control (Ethanol), and two experimental groups: high concentration Ac4ManNAc (100 uM) and high concentration Ac4ManNLev (100 uM). The aim is to gain insight into apoptosis and cell cycle arrest. Specifically, the Ac4ManNLev samples will be comprared to a less potent ManNAc analog. The RNA was amplified, labeled, and hybridized to the GLYCOv3 microarrays.

| S-ECPF-GEOD-28939 | biostudies-other

Fluvastatin-induced differential global gene expression in human metastatic MDA-MB-231 breast cancer cells

Project description:The current study analyzed the altered expression profiles of genes that are responsible for fluvastatin-induced breast cancer cell death in MDA-MB-231 cells (ER-ve basal breast cancer cells). Some of these altered gene expressions were further inter connceted to various pathways which may eventually be recognised as drug targets/ biomarkers in statin-sensitve breast cancer patients. To understand the differential gene expression profile in fluvastatin treated (24 h) malignant breast cancer cells with untreated malignant breast cancer cells.

| S-ECPF-GEOD-59007 | biostudies-other

Gene Expression Profiles Induced by High-dose Ionizing Radiation in MDA-MB-231 Triple-negative Breast Cancer Cell Line.

Project description:Background/aimRadiation therapy (RT) represents a therapeutic option in breast cancer (BC). Even if a great number of BC patients receive RT, not all of them report benefits, due to radioresistance that gets activated through several factors, such as the hormone receptor status. Herein, we analyzed the gene expression profiles (GEP) induced by RT in triple-negative BC (TNBC) MDA-MB-231, to study signalling networks involved in radioresistance.Materials and methodsGEP of MDA-MB-231 BC cells treated with a high dose of radiation, went through cDNA microarray analysis. In addition, to examine the cellular effects induced by RT, analyses of morphology and clonogenic evaluation were also conducted.ResultsA descriptive report of GEP and pathways induced by IR is reported from our microarray data. Moreover, the MDA-MB-231 Radioresistent Cell Fraction (RCF) selected, included specific molecules able to drive radioresistance.ConclusionIn summary, our data highlight, the RT response of TNBC MDA-MB-231 cell line at a transcriptional level, in terms of activating radioresistance in these cells, as a model of late-stage BC.

| S-EPMC6609258 | biostudies-literature

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