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Esophageal keratinocyte invasion after loss of E-cadherin and TGF receptor type II

ABSTRACT: Esophageal cancer is one of the deadliest cancers as patients present at late stages of disease. Frequent gene alterations include the loss of E-cadherin and TGFb receptor type II. The goal of this study was to establish a model of esophageal cancer by introducing dominant-negative mutants of E-cadherin and TGFb receptor II. To analyze the functional consequences and gene expression chages induced by E-cadherin and TGFb receptor type II loss in esophageal cancer.

ORGANISM(S): Homo sapiens

PROVIDER: GSE19472 | GEO | 2013/11/12

SECONDARY ACCESSION(S): PRJNA120349

REPOSITORIES: GEO

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Esophageal keratinocyte invasion after loss of E-cadherin and TGF receptor type II

Project description:Esophageal cancer is one of the deadliest cancers as patients present at late stages of disease. Frequent gene alterations include the loss of E-cadherin and TGFb receptor type II. The goal of this study was to establish a model of esophageal cancer by introducing dominant-negative mutants of E-cadherin and TGFb receptor II. To analyze the functional consequences and gene expression chages induced by E-cadherin and TGFb receptor type II loss in esophageal cancer. Human esophageal keratinocytes were retrovirally transfected with wild-type full length E-cadherin, dominant-negative E-cadherin and dominant-negative TGFb receptor type II. Grown in organotypic cultures on a collagen/matrigel matrix with embedded fibroblast, the generated cell lines were analyzed for their potential to invade into the underlying matrix. Each cell lines was grown in duplicate in organotypic culture and therefore 2 replicates analyzed. Gene expression changes in invasive versus non-invasive areas were analyzed after RNA isolation using laser-capture microdissection resulting in 2 samples representing a normal esophageal epithelium (Ecad), 2 each of dominant-negative Ecad (Ecyto) non-invasive and invasive. To model the genetic alterations in esophageal cancer dominant-negative E-cadherin and dominant-negative TGFb receptor type II (Ecyto-dnTGFR) were expressed and 2 samples each, non-invasive and invasive, analyzed.

2013-11-12 | E-GEOD-19472 | biostudies-arrayexpress

Homo sapiens

Project description:Esophageal keratinocyte invasion after loss of E-cadherin and TGF receptor type II

| PRJNA120349 | ENA

Effect of E-cadherin by N-cadherin replacement in mouse intestinal epithelial cells

Project description:We conditionally substituted E-cadherin (E-cad; cadherin 1) with N-cadherin (N-cad; cadherin 2) during intestine development by generating mice in which an Ncad cDNA was knocked into the Ecad locus We used microarray to follow gene expression changes derived from lack of E-cadherin on intestinal epithelial cells

2017-05-01 | GSE81920 | GEO

Bulk RNA sequencing of VE-Cadherin+GFP+, VE-Cadherin- GFP+ and VE-Cadherin+GFP- populations from E11.5 miR144/451+/GFP mouse yolk sac.

Project description:The aim of the experiment was to compare a newly defined population VE-Cadherin+GFP+ to control populations, VE-Cadherin- GFP+ and VE-Cadherin+GFP-.

2019-04-20 | GSE113403 | GEO

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

Project description: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.

2010-02-22 | GSE14943 | GEO

E-cadherin loss induces autocrine activation of oncogenic growth factor signalling in metastatic lobular breast cancer.

Project description:Background: Despite the fact that loss of E-cadherin is causal to the development and progression of invasive lobular breast cancer (ILC), no targeted therapy is available to treat this major breast cancer subtype. This study is aimed at identifying clinically targetable pathways that are aberrantly active downstream of E-cadherin loss in ILC. Methods: Reverse-phase protein array (RPPA) analyses were performed in the context of E-cadherin loss using mouse and human breast cancer cells. A combination of mRNA sequencing, conditioned medium growth assays and CRISPR-Cas9 knock-out experiments were performed to identify and validate activation of oncogenic pathways in ILC. Human ILC samples were employed to validate activation by immunohistochemistry on tissue micro-arrays. Finally, we assessed the effect of pathway inhibition using anoikis resistance and anchorage-dependent growth in vitro. Results: We demonstrate that E-cadherin loss leads to increased activation of FAK and PI3K/AKT signalling. Autocrine activation of growth factor receptor signalling and its downstream PI3K/AKT hub was a direct consequence of E-cadherin loss, independent of activating mutations in either PIK3CA, AKT or PTEN. Analysis of human ILC samples confirmed pathway activity, and pharmacological inhibition of AKT using AZD5363 and MK2206 resulted in robust inhibition of cell growth and survival of ILC cells in anchorage-dependent and independent conditions. Moreover, our results indicate a role for intracellular FAK in the regulation of ILC anoikis resistance. Conclusion: Our data demonstrate that E-cadherin loss evokes additional PI3K/AKT activation independent of oncogenic mutations in this pathway. We propose clinical intervention of PI3K/AKT in ILC based on functional E-cadherin inactivation, irrespective of activating pathway mutations.

2019-03-22 | GSE81977 | GEO

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.

2009-04-18 | GSE13362 | GEO

mRNA sequencing of breast cancer brain metastasis tumors FACS sorted for E-cadherin high and low levels

Project description:In this study we want to compare the expression profiles of E-cadherin high and low tumor cells from 4 different mice with breast cancer brain metastasis. We used a breast cancer brain metastasis model derived from the PyMT E-cadherin-mCFP breast cancer model (Beerling et al. Cell Reports 2016) and FACS sorted samples based on endogenous E-cadherin-mCFP expression.

2022-07-15 | GSE199775 | GEO

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

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

Circulating tumor cell-derived N-cadherin induces NK cell exhaustion and contributes to tumor self-seeding via the KLRG1 receptor

Project description:Circulating tumor cells (CTCs) can survive in the circulation and return to primary tumors through a self-seeding process. However, the mechanisms underlying CTC escape from natural killer (NK) cell-mediated immune surveillance remain unclear. In the present study, self-seeded tumor cells were isolated and characterized by applying a modified mouse model. The harvested self-seeded cells displayed resistance to NK cell-mediated lysis and a higher tumor seeding ability than their parental cells. Elevated expression levels of the CDH2 gene and its protein product, N-cadherin were found in self-seeded cell lines. We revealed an unrecognized role for soluble N-cadherin in inhibiting NK cell antitumor immunity. NK cells secreted cytokines, and fluid shear stress facilitated N-cadherin release from tumor cells by enhancing the activity of A disintegrin and metalloprotease 10 (ADAM10). Soluble N-cadherin triggered NK cell functional exhaustion by interacting with the killer cell lectin-like receptor subfamily G member 1 (KLRG1) receptor and therefore protected tumor cells from NK cell killing. Elevated N-cadherin expression was observed in recurrent oral cancer samples compared to matched primary tumors. Our findings illustrated an unknown mechanism by which CTCs evaded NK cell-mediated immune surveillance, which may contribute to tumor self-seeding and recurrence.

2022-09-21 | GSE186082 | GEO

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