Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

FRY Impacts Breast Cancer Malignancy by Inducing an Enrichment of Genes with Tumor-Suppressive Functions and Affecting EMT Potential of Breast Cancer Cells

ABSTRACT: Breast cancer is a disease with diverse phenotypes, and while the progression of breast cancer from a localized lesion to metastatic disease is well understood clinically. Our previous study genetically linked the FRY gene with differential susceptibility to mammary carcinogenesis; however, little is known about the mechanistic insights of FRY in mammalian cells and breast cancer progression. Through RNA-Seq analysis of series of constructed cell lines based on highly malignant triple-negative human breast cancer cells MDA-MB-231, we show that enhanced FRY induces massive changes in gene expression, which favor signalings and molecules with tumor-suppressive functions and engage in promoting cell differentiation, maintaining the normal and histopathological characteristics of epithelial cells, and in regulating EMT potential of breast cancer cells. As a result, the proliferation, migration and invasion potentials of breast cancer cells are significantly inhibited both in vitro and in xenograft tumor models. Importantly, consistent with FRY’s anti-tumor progression role, decreased FRY protein levels are correlated with poorly differentiated and aggressive tumor phenotypes in the analysis of two clinically annotated breast cancer cohorts. Our results identify FRY’s potent tumor-suppressive role at the gene transcription and molecular function levels, providing a novel biomarker for breast cancer prognosis and a target for therapeutic intervention.

ORGANISM(S): Homo sapiens

PROVIDER: GSE112910 | GEO | 2019/05/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Expression of FRY-targeting shRNA in MCF10A cells

Project description:We identified the predicted FRY gene as a candidate mammary carcinoma susceptibility gene. This gene has not been characterized in mammals, so for part of our analysis we conducted microarray experiments to look at the changes in gene expression which occur when FRY-targeting shRNA is expressed in the nontumorigenic MCF10A mammary epithelial cell line (a cell line which we identified as having higher FRY mRNA expression than breast cancer cell lines). We used microarrays to identify the FRY interactome and identified that FRY affects the expression of gene networks that maintain normal cellular and tissue architecture, organization, differentiation of epithelial cells.

2014-12-31 | GSE35928 | GEO

Ectopic expression of wild-type Cop Fry in MDA-MB-231 cells

Project description:We identified the wt Cop allele of the predicted Fry gene as a mammary carcinoma susceptibility gene. This gene has not been characterized in mammals, so for part of our analysis we conducted microarray experiments to look at the changes in gene expression which occur when the wt Cop Fry allele is ectopically expressed in the MDA-MB-231 breast cancer cell line (a cell line which we identified as having low FRY mRNA expression). We used microarrays to identify the Fry interactome and identified that Fry affects the expression of gene networks that maintain normal cellular and tissue architecture, organization, differentiation of epithelial cells.

2014-12-31 | GSE36441 | GEO

FRY Impacts Breast Cancer Malignancy by Inducing an Enrichment of Genes with Tumor-Suppressive Functions and Affecting EMT Potential of Breast Cancer Cells

Project description:FRY Impacts Breast Cancer Malignancy by Inducing an Enrichment of Genes with Tumor-Suppressive Functions and Affecting EMT Potential of Breast Cancer Cells

| PRJNA449466 | ENA

The RNA-binding protein RBM47 suppresses metastatic breast cancer progression

Project description:Through integrative analysis of clinical breast cancer gene expression datasets, cell line models of breast cancer progression, and mutation data from cancer genome resequencing studies, we have identified RNA binding motif protein 47 (RBM47) as a candidate suppressor of breast cancer metastasis. RBM47 inhibited breast cancer progression in experimental models. Transcriptome-wide analysis of RBM47 localization by HITS-CLIP revealed widespread binding to mRNAs, preferentially at the 3' UTRs. RBM47 altered the abundance of a subset of its target mRNAs. Some of the mRNAs stabilized by RBM47, as exemplified by dickkopf WNT signaling pathway inhibitor 1 (DKK1), mediate tumor suppressive effects downstream of RBM47. This work identifies RBM47 as a suppressor of breast cancer progression and highlights the potential of global RNA modulatory events as a source of metastasis-promoting phenotypic traits. Cancer cells transduced with doxycycline-inducible wildtype RBM47 or the RBM47-I281fs mutant, treated with increasing concentrations of doxycycline.

2014-06-11 | E-GEOD-53779 | biostudies-arrayexpress

The RNA-binding protein RBM47 suppresses metastatic breast cancer progression

2014-06-11 | GSE53779 | GEO

IL6/STAT3 co-opts ER regulatory elements to drive metastasis in breast cancer

Project description:Interleukin 6 (IL6) signaling has been associated with an aggressive and metastatic phenotype in multiple solid tumors including breast cancer, but its mechanism of action in mediating tumor progression and treatment response is not clear. By exploiting a clinically relevant intraductal xenograft model of estrogen receptor positive (ER+) breast cancer, we demonstrate that IL6 increases both primary tumor growth and distant metastases. By integrating pre-clinical models and clinical specimens, we show that signal transducer and activator of transcription 3 (STAT3) mediates IL6-induced activation of a metastatic gene program from enhancer-elements shared with ER and its pioneer factor FOXA1. Although IL6 activated STAT3 and ER/FOXA1 share cis-regulatory regions, STAT3 drives transcription independent of ER and FOXA1 function, and the IL6/STAT3 gene program is not influenced by ER-targeted therapies, decoupling these two important pathways. This demonstrates that ER/FOXA1 and IL6/STAT3 are two parallel, but independent actionable pathways controlling breast cancer progression.

2021-09-08 | PXD012980 | Pride

shRNA profiling of human normal breast and breast cancer cell lines to identify genes regulated by YAP

Project description:Frequent loss of heterozygosity (LOH) at 11q22-23 in breast cancer strongly suggests that this region contains a tumor suppressor gene, yet to be identified. We and others have shown Yes-associated protein (YAP), which is located at 11q22.2, transactivates the p53 family member p73 upon DNA damage, suggesting a tumor suppressive function for YAP. Our analysis of breast tumor tissues by immunohistochemistry (IHC) showed loss of YAP protein expression in great portion of breast cancers. We used microarray to look at the targte genes regulated by YAP in normal breast luminal cell and breast cancer cell lines. Experiment Overall Design: We generated stable cell lines by introducing control vector(pRS-IRES-GFP/pmig) or YAP shRNA(pRS-IRES-GFP-YAP/pmig-YAP) in a normal breast luminal cell line 1089 luminal and breast cancer cell lines MDA MB231. RAN was extracted and hybridized on Affymetrix microarrays.We looked for new target genes regulated by YAP in normal breast luminal cell and breast cancer cell lines.

2009-01-18 | E-GEOD-7700 | biostudies-arrayexpress

NLRP3 inflammasome in fibroblasts links tissue damage with inflammation in breast cancer progression and metastasis

Project description:Global gene expression of spontaneous breast tumors developed in transgenic mice at different time course (FVB/N-MMTV-PyMT: model of spontaneous mammary carcinoma. Lin EY et al.,Am J Pathol. 2003 Nov;163(5):2113-26. Cancer-Associated Fibroblasts (CAFs) are highly abundant in the microenvironment of breast tumors. CAFs were shown to orchestrate tumor-promoting inflammation in multiple malignancies, including breast cancer. However, the molecular pathways that govern the inflammatory role of CAFs are poorly characterized. In this study we found that fibroblasts can sense damage-associated molecular patterns (DAMPs), and in response activate the NLRP3 inflammasome pathway, resulting in instigation of pro-inflammatory signaling and secretion of IL-1β. This upregulation was evident in CAFs in mouse and in human breast carcinomas. Moreover, CAF-derived inflammasome signaling facilitated mammary tumor growth and lung metastasis, which was attenuated when NLRP3 or IL-1β were specifically ablated. Functionally, CAF-derived inflammasome promoted tumor progression and metastasis by modulating the tumor microenvironment towards an immune suppressive milieu and by upregulating the expression of adhesion molecules on endothelial cells. Thus, our findings elucidate a novel mechanism by which CAFs promote breast cancer progression and lung metastasis, by linking the physiological tissue damage response of fibroblasts with tumor-promoting inflammation.

2019-09-02 | GSE129189 | GEO

Genes regulated by YAP in normal breast cell line and breast cancer cell lines

2010-04-08 | GSE7700 | GEO

Mufudza2012 - Estrogen effect on the dynamics of breast cancer

Project description:Mufudza2012 - Estrogen effect on the dynamics of breast cancer This deterministic model shows the dynamics of breast cancer with immune response. The effects of estrogen are incorporated to study its effects as a risk factor for the disease. This model is described in the article: Assessing the effects of estrogen on the dynamics of breast cancer. Mufudza C, Sorofa W, Chiyaka ET. Comput Math Methods Med 2012; 2012: 473572 Abstract: Worldwide, breast cancer has become the second most common cancer in women. The disease has currently been named the most deadly cancer in women but little is known on what causes the disease. We present the effects of estrogen as a risk factor on the dynamics of breast cancer. We develop a deterministic mathematical model showing general dynamics of breast cancer with immune response. This is a four-population model that includes tumor cells, host cells, immune cells, and estrogen. The effects of estrogen are then incorporated in the model. The results show that the presence of extra estrogen increases the risk of developing breast cancer. This model is hosted on BioModels Database and identified by: BIOMD0000000642. To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information.

2024-09-02 | BIOMD0000000642 | BioModels

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data