Role Of E-cadherin Research Articles

Expression and prognostic value of E-cadherin in laryngeal cancer

Conclusion: Down-regulation of ECD may associate with infiltrative tumor growth and result in poor prognosis. However, ECD expression is not significantly associated with tumor metastasis. Aim: To investigate the prognostic role of E-cadherin (ECD) expression in laryngeal cancer. Methods: In a clinical study, a total of 79 laryngeal cancer patients who received surgery were included in this study. The expression of ECD in laryngeal cancer tissue was detected by immumohistochemical staining. In an in vitro study, ECD up-regulated cells (Ad-ECD) and ECD down-regulated cells (sh-ECD) were cultured, along with interference by siRNA. Cell apoptosis was detected by flow cytometry. In an in vivo study, nude mice were injected with Ad-ECD, sh-ECD, and Hep-2 cells. The ECD expression and tumor metastasis in the brain, liver, and lung tissues were detected. Results: Clinical data showed that expression of ECD was statistically correlated with survival rate (p < 0.05), but not with other clinical characteristics, such as age, gender, lymphatic metastasis, and TNM staging. ECD was down-regulated in sh-ECD cells and the down-regulation significantly reduced apoptosis of Hep-2 cells. Tumor growth was significantly inhibited in the Ad-ECD group. Except the tumor tissue, no positive ECD expression or significant tumor cells were found in the brain, liver, and lung tissues.

609 Role of E-Cadherin of Dendritic Cells in Colonic Homeostasis

609 Role of E-Cadherin of Dendritic Cells in Colonic Homeostasis

782 A Tumor Suppressive Role for E-Cadherin in a New Model of Metastatic Gastric Cancer

782 A Tumor Suppressive Role for E-Cadherin in a New Model of Metastatic Gastric Cancer

Abstract P2-05-12: Epithelial paradox; clinical significance of co-expression of E-cadherin and vimentin in invasive breast cancer

Abstract Background: E-cadherin and vimentin are now regarded as major and conventional canonical markers of epithelial-mesenchymal transition (EMT). It is commonly assumed E-cadherin is uniformly lost during the process of EMT. We previously reported that the elevated expression of vimentin contributes to the aggressive phenotype in invasive breast cancer. On the other hand, the role of E-cadherin in breast cancer biology might be unclear and more complex. Although, cell cohesion during breast cancer invasion is often overlooked, accumulating evidences indicate breast tumor cells are typically cohesive and often display membrane-localized E-cadherin in both the primary tumor and distant metastases, termed collective invasion. Multiple mechanisms have emerged to address how epithelial breast tumors invade. Aims: The aim of this study is to reveal the clinical importance of the expression of E-cadherin and vimentin in breast cancer. Methods: The E-cadherin and vimentin protein expression were evaluated by immunohistochemistry (IHC) in 177 invasive breast cancer samples. Among these, E-cadherin and vimentin expression were evaluated in the set of primary breast cancer and metastatic lymph nodes in 65 cases. Results: The positive vimentin expression was highly correlated with poor disease-free survival (DFS) and overall survival (OS) (p=0.019 and p=0.0044), however, the E-cadherin expression alone did not correlate with prognosis. Interestingly, Both E-cadherin and vimentin positive tumor had the worst DFS and OS among all breast cancer (p=0.03 and p=0.0089). Vimentin expression was highly correlated between primary tumors and metastatic lymph nodes. However, E-cadherin expression levels were significantly elevated in metastatic lymph nodes (p=0.0017), Co-expression of E-cadherin and vimentin in the metastatic lymph nodes also showed worst DFS and OS (p=0.12 and p=0.027). Conclusions: Co-expression of E-cadherin and vimentin seems to be associated with the most aggressive phenotype and poorest prognosis in breast cancer, and positive E-cadherin expression may not always play roles for tumor suppression. Citation Format: Yamashita N, Tokunaga E, Inoue Y, Tanaka K, Ueo H, Saeki H, Oki E, Maehara Y. Epithelial paradox; clinical significance of co-expression of E-cadherin and vimentin in invasive breast cancer. [abstract]. In: Proceedings of the Thirty-Eighth Annual CTRC-AACR San Antonio Breast Cancer Symposium: 2015 Dec 8-12; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2016;76(4 Suppl):Abstract nr P2-05-12.

The role of E-cadherin - 160C/A polymorphism in breast cancer

AbstractBreast cancer is the most prevalent cancer in women worldwide. Numerous studies have suggested that the E-cadherin adhesion system is dysregulated in cancer cells. These impaired functions of E-cadherin contribute to releasing cancer cells from the primary lesion to cell dedifferentiation. Some studies have shown that polymorphism may affect E-cadherin expression, and then play a role in susceptibility to breast cancer. However, the results remained controversial. In this short review, we summarize the functions of E-cadherin and the signaling pathways it regulates, and assess the association between CDH1 polymorphisms and breast cancer susceptibility. This study suggests that genetic variation in CDH1 and -160C/A polymorphism may have an association with breast cancer risk. The assessment of CDH1 polymorphisms may be used for the identification of patients suitable for anti- CDH1 therapy.

The Role of E-Cadherin in Maintaining the Barrier Function of Corneal Epithelium after Treatment with Cultured Autologous Oral Mucosa Epithelial Cell Sheet Grafts for Limbal Stem Deficiency.

The role of E-cadherin in epithelial barrier function of cultured autologous oral mucosa epithelial cell sheet (CAOMECS) grafts was examined. CAOMECS were cultured on a temperature-responsive surface and grafted onto rabbit corneas with Limbal Stem Cell Deficiency (LSCD). E-cadherin levels were significantly higher in CAOMECS compared to normal and LSCD epithelium. Beta-catenin colocalized with E-cadherin in CAOMECS cell membranes while phosphorylated beta-catenin was significantly increased. ZO-1, occludin, and Cnx43 were also strongly expressed in CAOMECS. E-cadherin and beta-catenin localization at the cell membrane was reduced in LSCD corneas, while CAOMECS-grafted corneas showed a restoration of E-cadherin and beta-catenin expression. LSCD corneas did not show continuous staining for ZO-1 or for Cnx43, while CAOMECS-grafted corneas showed a positive expression of ZO-1 and Cnx43. Cascade Blue® hydrazide did not pass through CAOMECS. Because E-cadherin interactions are calcium-dependent, EGTA was used to chelate calcium and disrupt cell adhesion. EGTA-treated CAOMECS completely detached from cell culture surface, and E-cadherin levels were significantly decreased. In conclusion, E cadherin high expression contributed to CAOMECS tight and gap junction protein recruitment at the cell membrane, thus promoting cellular adhesion and a functional barrier to protect the ocular surface.

A role for E-cadherin in ensuring cohesive migration of a heterogeneous population of non-epithelial cells.

Collective cell migration is a key process underlying the morphogenesis of many organs as well as tumour invasion, which very often involves heterogeneous cell populations. Here we investigated how such populations can migrate cohesively in the Drosophila posterior midgut, comprised of epithelial and mesenchymal cells and show a novel role for the epithelial adhesion molecule E-cadherin (E-Cad) in mesenchymal cells. Despite a lack of junctions at the ultrastructure level, reducing E-Cad levels causes mesenchymal cells to detach from one another and from neighbouring epithelial cells; as a result, coordination between the two populations is lost. Moreover, Bazooka and recycling mechanisms are also required for E-Cad accumulation in mesenchymal cells. These results indicate an active role for E-Cad in mediating cohesive and ordered migration of non-epithelial cells, and discount the notion of E-Cad as just an epithelial feature that has to be switched off to enable migration of mesenchymal cells.

E-cadherin and Src associate with extradesmosomal Dsg3 and modulate desmosome assembly and adhesion.

Desmosomes provide strong intercellular cohesion essential for the integrity of cells and tissues exposed to continuous mechanical stress. For desmosome assembly, constitutively synthesized desmosomal cadherins translocate to the cell-cell border, cluster and mature in the presence of Ca(2+) to stable cell contacts. As adherens junctions precede the formation of desmosomes, we investigated in this study the relationship between the classical cadherin E-cadherin and the desmosomal cadherin Desmoglein 3 (Dsg3), the latter of which is indispensable for cell-cell adhesion in keratinocytes. By using autoantibodies from patients with the blistering skin disease pemphigus vulgaris (PV), we showed in loss of function studies that E-cadherin compensates for effects of desmosomal disassembly. Overexpression of E-cadherin reduced the loss of cell cohesion induced by PV autoantibodies and attenuated activation of p38 MAPK. Silencing of E-cadherin abolished the localization of Dsg3 at the membrane and resulted in a shift of Dsg3 from the cytoskeletal to the non-cytoskeletal protein pool which conforms to the notion that E-cadherin regulates desmosome assembly. Mechanistically, we identified a complex consisting of extradesmosomal Dsg3, E-cadherin, β-catenin and Src and that the stability of this complex is regulated by Src. Moreover, Dsg3 and E-cadherin are phosphorylated on tyrosine residues in a Src-dependent manner and Src activity is required for recruiting Dsg3 to the cytoskeletal pool as well as for desmosome maturation towards a Ca(2+)-insensitive state. Our data provide new insights into the role of E-cadherin and the contribution of Src signaling for formation and maintenance of desmosomal junctions.

Clinical significance of co-expression of E-cadherin and vimentin in invasive breast cancer.

e22013 Background: E-cadherin has been categorized as a tumor suppressor and its downregulation is considered to occur in the process of epithelial-mesenchymal transition (EMT). E-cadherin and vimentin are now regarded as major and conventional canonical markers of EMT. We previously reported that the elevated expression of vimentin contributes to the aggressive phenotype in invasive breast cancer. However, the role of E-cadherin in breast cancer biology might be unclear and more complex. The aim of this study is to reveal the clinical importance of the expression of E-cadherin and vimentin in breast cancer. Methods: The E-cadherin and vimentin protein expression were evaluated by immunohistochemistry (IHC) in 176 invasive breast cancer samples. Among these, E-cadherin and vimentin expression were evaluated in the set of primary breast cancer and metastatic lymph nodes in 65 cases. Results: The positive vimentin expression was highly correlated with poor disease-free survival (DFS) and overall survival (OS) (p = 0.019 and p = 0.0044), however, the E-cadherin expression alone did not correlate with prognosis. Interestingly, Both E-cadherin and vimentin positive tumor had the worst DFS and OS among all breast cancer (p = 0.03 and p = 0.0089). Vimentin expression was highly correlated between primary tumors and metastatic lymph nodes. However, E-cadherin expression levels were significantly elevated in metastatic lymph nodes (p = 0.0017), Co-expression of E-cadherin and vimentin in the metastatic lymph nodes also showed worst DFS and OS (p = 0.12 and p = 0.027). Conclusions: Co-expression of E-cadherin and vimentin seems to be associated with the most aggressive phenotype and poor prgnosis in breast cancer, and positive E-cadherin expression may not always play roles for tumor suppression.

Adhesion in mammary development: novel roles for E-cadherin in individual and collective cell migration.

Epithelial tissues are essential for barrier function, secretion, and regulation of fluid transport. Their function requires cell polarity and cell-cell adhesion, mediated through intercellular junctions. Conversely, disruption of adhesion and polarity is thought to drive cancer progression. The mammary gland is an important model for cell adhesion due to its postnatal hormonally regulated development; ducts undergo branching morphogenesis in response to steroid hormones during puberty. These hormonal signals induce a transition from simple to stratified architecture, initiated by asymmetric luminal cell divisions. Ductal elongation is accomplished by this multilayered, low-polarity epithelium, and polarity is reestablished as elongation ceases. The requirement for cell adhesion has been tested in 3D culture and in vivo, using gene deletion, knockdown, and misexpression in both developmental and homeostatic contexts. Attention has focused on E-cadherin, the major classical cadherin in luminal epithelial cells. Classic studies revealed a requirement for E-cadherin during lactation, and E-cadherin loss is widely posited to promote metastasis. However, recent findings demonstrated a broader requirement for E-cadherin during branching morphogenesis and homeostasis and also, surprisingly, in epithelial dissemination. These studies suggest that long-standing models of the role of adhesion in epithelial biology need to be revisited. Advances in inducible gene expression and knockdown, CRISPR/Cas9 technology, and fluorescent labeling of genetically modified cells offer the opportunity to test the roles of diverse adhesion systems and to develop a mechanistic understanding of how cell adhesion regulates development and cancer.

E-cadherin Immunohistochemistry Stain and Acute Erythroid Leukemia, the Emerging Story

E-Cadherin is calcium-dependent cell adhesion molecule encoded by CDH1 gene at chromosome 16q22.1. Ecadherin regulates cell-cell adhesions and controls mobility and proliferation of epithelial cells. Recently, the role of E-cadherin in erythroid maturation has been elucidated. It is selectively expressed in immature erythroblasts and gradually down regulated as erythroid precursors mature. Acute erythroid leukemia is neoplastic proliferation of immature erythroid precursors in bone marrow with or without significant myeloblasts component. In the recent years E-cadherin has emerged as the most sensitive and specific marker for immature erythroblasts. Moreover, combination of E-cadherin with glycophorin A in immunohistochemistry staining can effectively separate immature vs. mature erythroid precursors in bone marrow biopsy. In this short review I will shed light on the key points related to the nature of relationship between E-cadherin and acute erythroid leukemia.

Role of E-cadherin in psoriasis

Role of E-cadherin in psoriasis

Cellular and molecular mechanisms of single and collective cell migrations in Drosophila: themes and variations.

The process of cell migration is essential throughout life, driving embryonic morphogenesis and ensuring homeostasis in adults. Defects in cell migration are a major cause of human disease, with excessive migration causing autoimmune diseases and cancer metastasis, whereas reduced capacity for migration leads to birth defects and immunodeficiencies. Myriad studies in vitro have established a consensus view that cell migrations require cell polarization, Rho GTPase-mediated cytoskeletal rearrangements, and myosin-mediated contractility. However, in vivo studies later revealed a more complex picture, including the discovery that cells migrate not only as single units but also as clusters, strands, and sheets. In particular, the role of E-Cadherin in cell motility appears to be more complex than previously appreciated. Here, we discuss recent advances achieved by combining the plethora of genetic tools available to the Drosophila geneticist with live imaging and biophysical techniques. Finally, we discuss the emerging themes such studies have revealed and ponder the puzzles that remain to be solved.

Abstract 3166: Rab11 regulates E-cadherin expression and induces cell transformation in colorectal carcinoma

Abstract In the process of epithelial mesenchymal transition EMT, the disassembly of junctional adhesion complexes such as E-cadherin is a remarkable sign during changes in cell morphology and polarity. However, E-cadherin expression is dynamic, and is regulated by the cellular endocytic system; it is also involved in cell signaling mechanisms. In this study, we investigated the role of E-cadherin in colorectal tumors and the relationship with recycling endosome protein Rab11 in colon cell transformation. For tissue screening, the expressions of E-cadherin and Rab11 in colorectal tumors were identified by immunohistochemistry in 113 patients with colorectal carcinoma. For the in vitro cell experiment, GFP-tagged Rab11 plasmid was transfected into HT29 colon cells, E-cadherin expression and cell transformation were monitored by Western blot and confocal microscopy. In immunohistochemistry, the mean score of E-cadherin in tumor and normal tissues was 1.41 ± 0.06 and 1.08 ± 0.06 (p &amp;lt; 0.05). The mean score of Rab11 in tumor and normal tissues was 0.51 ± 0.05 and 0.18 ± 0.02 (p &amp;lt; 0.05). Synchronous overexpression of E-cadherin and Rab11 was noted in 74 patients (66.5%) with colorectal carcinoma. When GFP-tagged Rab11 plasmid was overexpressed in cultured colon cell line HT-29, the E-cadherin expression was up-regulated, and a fibroblast-like cell polarity was induced, which resulted in cell transformation. This study demonstrated the importance of the overexpression of Rab11 and E-cadherin in colorectal cancer. The results indicated that Rab11 together with E-cadherin might be potential markers for colorectal cancer progression and treatment. Citation Format: Yuan-Chiang Chung, Wan-Chen Wei, Shin-Han Huang, Chi-Min Shih, Chih-Ping Hsu, King-Jen Chang, Wei-Ting Chao. Rab11 regulates E-cadherin expression and induces cell transformation in colorectal carcinoma. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 3166. doi:10.1158/1538-7445.AM2014-3166

From cell membrane to the nucleus: an emerging role of E-cadherin in gene transcriptional regulation.

E-cadherin is a well-known mediator of cell–cell adherens junctions. However, many other functions of E-cadherin have been reported. Collectively, the available data suggest that E-cadherin may also act as a gene transcriptional regulator. Here, evidence supporting this claim is reviewed, and possible mechanisms of action are discussed. E-cadherin has been shown to modulate the activity of several notable cell signalling pathways, and given that most of these pathways in turn regulate gene expression, we proposed that E-cadherin may regulate gene transcription by affecting these pathways. Additionally, E-cadherin has been shown to accumulate in the nucleus where documentation of an E-cadherin fragment bound to DNA suggests that E-cadherin may directly regulate gene transcription. In summary, from the cell membrane to the nucleus, a role for E-cadherin in gene transcription may be emerging. Studies specifically focused on this potential role would allow for a more thorough understanding of this transmembrane glycoprotein in mediating intra- and intercellular activities.

Roles of E-cadherin (CDH1) genetic variations in cancer risk: a meta-analysis.

E-Cadherin (CDH1) genetic variations may be involved in invasion and metastasis of various cancers by altering gene transcriptional activity of epithelial cells. However, published studies on the association of CDH1 gene polymorphisms and cancer risk remain contradictory, owing to differences in living habits and genetic backgrounds. To derive a more better and comprehensive conclusion, the present meta-analysis was performed including 57 eligible studies of the association between polymorphisms of CDH1 gene promoter -160 C>A, -347 G>GA and 3'-UTR +54 C>T and cancer risk. Results showed that these three polymorphisms of CDH1 were significantly associated with cancer risk. For -160 C>A polymorphism, -160A allele carriers (CA and CA+AA) had an increased risk of cancer compared with the homozygotes (CC), and the similar result was discovered for the -160A allele in the overall analyses. In the subgroup analyses, obvious elevated risk was found with -160A allele carriers (AA, CA, CA+AA and A allele) for prostate cancer, while a decreased colorectal cancer risk was shown with the AA genotype. For the -347 G>GA polymorphism, the GAGA genotype was associated with increased cancer risk in the overall analysis with homozygous and recessive models. In addition, results of subgroup analysis indicated that the elevated risks were observed in colorectal cancer and Asian descendants. For +54 C>T polymorphism, a decreased risk of cancer was found in heterozygous, dominant and allele models. Moreover, +54T allele carriers (CT, CT+TT genotype and T allele) showed a potential protective factor in gastric cancer and Asian descendants.

MP31-13 THE EXPRESSION AND FUNCTION OF FAM110A IN HUMAN PROSTATE CANCER

INTRODUCTION AND OBJECTIVES: The loss of cell-cell contacts between epithelial cells is an important step in cancer progression. Alpha-catenin plays a crucial role in E-cadherin mediated cell-cell adhesion. We identified a novel protein FAM110A that interacts with alpha-catenin. FAM110A is a member of FAM110 gene family that was originally identified in a search for centrosome and spindle pole-associated proteins, but whose function in cancer is still unknown. We hypothesized that FAM110A plays a role in prostate cancer (PrCa) progression. The objective of this study is to analyze the expression and biological functions of FAM110A in PrCa. METHODS: Expression of the FAM110A gene in tumor cell lines and in human PrCa tissues was analyzed by quantitative real-time PCR. We created an EGFP-tagged FAM110A expression vector to observe the localization of FAM110A in cancer cells. Co-immunoprecipitation experiments were performed to confirm the genuine interaction between FAM110A and alpha-catenin. We established a doxycycline-inducible FAM110A expressing A431 cell line. This cell line was used to study the effect of FAM110A on cell viability, migration and invasion, using CellTiter-Glo , wound healing and Matrigel invasion assays, respectively. RESULTS: In human prostate tissues, we found that FAM110A mRNA expression in primary PrCa was unchanged, but was significantly increased in PrCa metastasis (1.5-fold increase compared to normal prostate tissue, p1⁄40.037). The immunofluorescence staining showed that FAM110A was co-localized with E-cadherin and betacatenin at cell-cell adherence junctions. In doxycycline-inducible FAM110A cells, FAM110A did neither affect cell viability nor cell migration, but cell invasiveness was significantly increased after FAM110A induction (1.9-fold compared to non-induced cells, p1⁄40.002). FAM110A expressing cells had a more spindle-like cell morphology, and had impaired F-actin bundle formation. CONCLUSIONS: FAM110A gene expression analysis in prostate tissues suggests that FAM110A plays a role in PrCa metastasis. Furthermore, results of functional assays indicate that binding of FAM110A to alpha-catenin may change the interaction between alpha-catenin and the actin cytoskeleton, which results in a more mesenchymal-like cell morphology and the acquisition of an invasive phenotype.

The Curses and the Blesses of E-Cadherin

E-cadherin is an evolutionary conserved molecule expressing from lower level animal to human. The principal role of E-cadherin is to maintain appropriate cell-cell connectivity at adherensjunction. Besides its role as cell-cell connector protein, E-cadherin is integrally involved in intracellular signaling as well as cytoskeletal remodeling. Proper spaciotemporal regulations as well as relevant specialized functions of E-cadherin are important for maintaining normal embryogenesis, cellular morphology and physiological function. However, defects in the expression and function of this gene products could become curses since numerous genetic and developmental studies have identified the critical role of this gene in path physiological conditions of multiple types of cancers leading to fatality. Recent study identified essential role of this gene product in stem cell biology including normal embryogenesis, induced pluripotent stem cell (iPSC) generation and stem cell differentiation. Currently iPSC has become a prime choice as starting material for regenerative medicine to treat many diseases; however the relevant technology has many shortcomings. Our lab and others have been exploiting this protein for successful application in regenerative medicine that made it a blessed molecule. Here, based on the latest available information, we are concisely presenting these agonies and advantages of E-cadherin.

Abstract C39: Building a novel molecular model for Twist1-induced epithelial dissemination

Abstract Most solid tumors originate from epithelial cells, and their metastasis represents the major cause of death among cancer patients. Because each tumor contains many mutations, it has been difficult to isolate how individual genetic events contribute to a tumor cell's ability to disseminate. Two posited mechanisms for metastasis are loss of cell-cell adhesion and activation of an epithelial-mesenchymal transition (EMT). These molecular models converge on the cell adhesion gene E-cadherin (Cdh1). E-cadherin is frequently mutated in human cancers, and it can also be transcriptionally repressed during EMT. In turn, expression of EMT transcription factors in multiple epithelial cancers has been correlated with increased invasion and metastasis. However, the acute consequences of E-cadherin loss or EMT activator expression in otherwise normal epithelial tissues remain incompletely understood. We therefore utilized a combination of organotypic culture, Cre-lox based gene deletion, inducible expression systems, and time-lapse imaging to test the sufficiency of single genetic perturbations to induce dissemination in primary murine mammary epithelium. E-cadherin deletion induced loss of simple epithelial architecture and inhibited branching morphogenesis in 3D culture and in vivo. Furthermore, E-cadherin loss acutely induced collective invasion past basement membrane. However, E-cadherin- cells remained non-protrusive, adhered to one another, and rarely disseminated. Conversely, expression of the EMT transcription factor Twist1 induced rapid dissemination of individual epithelial cells into the extracellular matrix (ECM), and disseminated cells proliferated to form secondary sites. Surprisingly, Twist1+ cells were observed to have membrane-localized E-cadherin during dissemination and during migration in the ECM. Our data thus provide distinct roles for E-cadherin and Twist1 in the early cellular processes of metastasis. We are currently testing whether shRNA knockdown of E-cadherin synergizes with Twist1 to further enhance dissemination. To date, we have demonstrated the sufficiency of constitutive Twist1 expression to induce dissemination of both major mammary cell types: inner luminal epithelial cells and outer myoepithelial cells. Moreover, we observe abnormal localization of myoepithelial cells and basement membrane to the inside of the tissue. However, it remains unclear why some Twist1-expressing cells disseminate while many others remain in the epithelium. We hypothesize that intrinsic, cell type-specific factors influence disseminative capacity. We next seek to test the sufficiency of Twist1 to induce cell dissemination and secondary site formation in distinct mammary epithelial subpopulations. We have developed mouse models that use cell-type specific promoters to drive Twist1 expression in myoepithelial, luminal progenitor, and differentiated luminal lineages. We anticipate that differences across cell types may help identify the subpopulations within a heterogeneous tumor with the highest metastatic potential. Furthermore, we expect that extrinsic factors, such as normal myoepithelial cells, may restrict dissemination of Twist1-expressing luminal cells. Understanding such modulation of Twist1's phenotypic outcomes could suggest new approaches to suppressing metastasis without necessitating direct inhibition of Twist1, itself an “undruggable” target. Citation Format: Eliah R. Shamir, Phuoc T. Tran, Andrew J. Ewald. Building a novel molecular model for Twist1-induced epithelial dissemination. [abstract]. In: Proceedings of the Third AACR International Conference on Frontiers in Basic Cancer Research; Sep 18-22, 2013; National Harbor, MD. Philadelphia (PA): AACR; Cancer Res 2013;73(19 Suppl):Abstract nr C39.

Gene of the month: E-cadherin (CDH1)

Epithelial-cadherin (E-cadherin; encoded by CDH1 ) is a member of the classical cadherins (the others being neural cadherin (N-cadherin) and vascular endothelial cadherin (VE-cadherin)). These single-pass transmembrane glycoproteins are expressed...