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Cadherin-11 depletion in aggressive MDA-MB-231 breast cancer cells.

ABSTRACT: Cadherin-11 expression is associated with tumor progression and metastasis in various cancers, including basal-like breast carcinoma and advanced prostate cancer, and invasive cell lines, yet is absent in normal epithelium. We now show cadherin-11 attenuation in aggressive breast and prostate cancer cells results in marked decreases in proliferation, migration, and invasion. Cadherin-11 depletion in MDA-231 cells prevents tumor growth in mice and alters gene expression associated with poor prognosis malignancies. Additionally, a novel small molecule inhibitor targeting its unique adhesive interface significantly inhibits the growth and migration of cadherin-11 positive cells. Cadherin-11 is essential for malignant progression of MDA-231 basal-type cells, and may serve as both an aggressive tumor marker and viable therapeutic target for poor prognosis carcinomas expressing it.

ORGANISM(S): Homo sapiens

PROVIDER: GSE14943 | GEO | 2010/02/22

SECONDARY ACCESSION(S): PRJNA111987

REPOSITORIES: GEO

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Homo sapiens

Project description:Cadherin-11 depletion in aggressive MDA-MB-231 breast cancer cells.

| PRJNA111987 | ENA

Oct4 affects E-cadherin expression via regulating Rnd1 associated cytoskeleton rearrangement in breast cancer cells

Project description:Oct4, a key transcription factor for maintaining the pluripotency and self-renewal of stem cells has been reported previously. It also plays an important role in tumor proliferation and apoptosis, but the role of Oct4 been in tumor metastasis is still not very clear. Here, we found that ectopic expression of Oct4 in breast cancer cells can inhibit their migration and invasion. Detailed examinations revealed that Oct4 up-regulates expression of E-cadherin, indicative of its inhibitory role in epithelial-mesenchymal transition (EMT). RNA-sequence assay showed that Oct4 down-regulates expression of Rnd1. As an atypical Rho protein, Rnd1 can affect cytoskeleton rearrangement and regulate cadherin-based cell-cell adhesion by antagonizing the typical Rho protein, RhoA. Ectopic expression of Rnd1 in MDA-MB-231 cells changes cell morphology which influences cell adhesion and increases migration. It is reported that EMT is accompanied by cytoskeleton remodeling, we hypothesized that Rnd1 may play a role in regulating EMT. Over-expression of Rnd1 can partly rescue the inhibitory effects induced by Oct4, not only migration and invasion, but also in E-cadherin level and cellular morphology. Furthermore, silencing of Rnd1 can up-regulate the expression of E-cadherin in MDA-MB-231 cells. These results present evidence that ectopic expression of Oct4 increases E-cadherin and inhibits metastasis, effects which may be related to Rnd1 associated cell-cell adhesion in breast cancer cells. Examination of mRNA profiles in MDA-MB-231 cells with OCT4 overexpressing

2014-01-25 | E-GEOD-54392 | biostudies-arrayexpress

Functional characterization of E- and P-cadherin in invasive breast cancer cells

Project description:Alterations in the cadherin-catenin adhesion complexes are involved in tumor initiation, progression and metastasis. However, the functional implication of distinct cadherin types in breast cancer biology is still poorly understood. Methods: To compare the functional role of E-cadherin and P-cadherin in invasive breast cancer, we stably transfected these molecules into the MDA-MB-231 cell line, and investigated their effects on motility, invasion and gene expression regulation. Expression of either E- and P-cadherin significantly increased cell aggregation and induced a switch from fibroblastic to epithelial morphology. Although expression of these cadherins did not completely reverse the mesenchymal phenotype of MDA-MB-231 cells, both E- and P-cadherin decreased fibroblast-like migration and invasion through extracellular matrix in a similar way. Moreover, microarray gene expression analysis of MDA-MB-231 cells after expression of E- and P-cadherins revealed that these molecules can activate signaling pathways leading to significant changes in gene expression. Although the expression patterns induced by E- and P-cadherin showed more similarities than differences, 40 genes were differentially modified by the expression of either cadherin type. Microarray gene expression analysis of MDA-MB-231 cells after expression of E- and P-cadherins using different clones for each conditions to reveal that these molecules can activate signaling pathways leading to significant changes in gene expression

2010-06-19 | E-GEOD-13362 | biostudies-arrayexpress

Expression data from ELK3 knocked down MDA-MB-231 cell line.

Project description:Triple-negative breast cancer is a highly aggressive tumor subtype that lacks effective therapeutic targets. Here, we show that ELK3 is overexpressed in a subset of breast cancers, in particular basal-like and normal-like/claudin-low cell lines. Suppression of ELK3 in MDA-MB-231 cells led to transdifferentiation from an invasive mesenchymal phenotype to a non-invasive epithelial phenotype both in vitro and in vivo. Suppression of ELK3 results in the extensive changes in genome expression profiles. Among these, GATA3, a master suppressor of metastasis, was epigenetically activated and we found that suppression of GATA3 led to the restoration of migration and invasion. These results suggest that the ELK3-GATA3 axis is a major pathway that promotes metastasis of MDA-MB-231 cells. Retrovirus expressing shRNA of ELK3 was transduced into MDA-MB-231 cell line and stable cell line of which ELK3 is suppressed more than 50% was selected by the drug selection (Puromycin).

2016-06-15 | E-GEOD-83325 | biostudies-arrayexpress

Functional characterization of E- and P-cadherin in invasive breast cancer cells

2009-04-18 | GSE13362 | GEO

Expression data from ELK3 knocked down MDA-MB-231 cell line.

2016-06-15 | GSE83325 | GEO

Oct4 affects E-cadherin expression via regulating Rnd1 associated cytoskeleton rearrangement in breast cancer cells

2014-01-25 | GSE54392 | GEO

ITIH5

Project description:In order to identify patterns of gene expression that are associated with the putative tumor suppressor gene ITIH5 mediated suppression of breast cancer metastatic growth, we performed a transcriptomic micro-array analysis of the MDA-MB-231 wildtype, three independent highly aggressive MDA-MB-231-mock clones and four independent weak aggressive MDA-MB-231-ITIH5 clones. Related methylation profiling data are found under accession <a href='../E-MTAB-5081/'>E-MTAB-5081</a>.

2017-01-30 | E-MTAB-1813 | biostudies-arrayexpress

Genome-wide profiles of multiple histone modifications in MDA-MB-231 and LM2-4175 cell lines

Project description:LM2-4175 cell line was originally selected from MDA-MB-231,but has more aggressive characteristics in invasion, migration and metastasis. In addition, LM2 cell line specifically metastasizes to lung. To understand the regulatory mechanisms of lung metastasis in breast cancer, we analyzed the chromatin structure of MDA-MB-231 and LM2-4175 cell lines.

2019-07-31 | GSE124379 | GEO

Next generation sequencing analysis of transcriptomes in MDA-MB-231 and LM2-4175 cell lines

Project description:LM2-4175 cell line was originally selected from MDA-MB-231,but has more aggressive characteristics in invasion, migration and metastasis. In addition, LM2 cell line specifically metastasizes to lung. To understand the melecular mechanisms of lung metastasis in breast cancer,we analyzed the RNA-seq data of MDA-MB-231 and LM2-4175 cell lines.

2019-07-31 | GSE124380 | GEO

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