scholarly journals The Autophagic Route of E-Cadherin and Cell Adhesion Molecules in Cancer Progression

Cancers ◽  
2021 ◽  
Vol 13 (24) ◽  
pp. 6328
Author(s):  
Manuela Santarosa ◽  
Roberta Maestro
Keyword(s):  
Cell Adhesion ◽  
Adhesion Molecules ◽  
Cancer Progression ◽  
Cell Adhesion Molecules ◽  
Epithelial To Mesenchymal Transition ◽  
Cell Transformation ◽  
Epithelial Tissue ◽  
Mesenchymal Transition ◽  
Intracellular Degradation ◽  
E Cadherin

Cell-to-cell adhesion is a key element in epithelial tissue integrity and homeostasis during embryogenesis, response to damage, and differentiation. Loss of cell adhesion and gain of mesenchymal features, a phenomenon known as epithelial to mesenchymal transition (EMT), are essential steps in cancer progression. Interestingly, downregulation or degradation by endocytosis of epithelial adhesion molecules (e.g., E-cadherin) associates with EMT and promotes cell migration. Autophagy is a physiological intracellular degradation and recycling process. In cancer, it is thought to exert a tumor suppressive role in the early phases of cell transformation but, once cells have gained a fully transformed phenotype, autophagy may fuel malignant progression by promoting EMT and conferring drug resistance. In this review, we discuss the crosstalk between autophagy, EMT, and turnover of epithelial cell adhesion molecules, with particular attention to E-cadherin.

scholarly journals ANALYSIS OF E-CADHERIN EXPRESSION IN A GROUP OF PRIMARY CUTANEOUS SQUAMOUS CELL CARCINOMAS

2019 ◽  
Vol 2 (2) ◽  
Author(s):  
Andreea Calinescu ◽  
Cristian Scheau ◽  
Sabina Zurac ◽  
Roxana Ioana Nedelcu ◽  
Alice Brinzea ◽  
...  
Keyword(s):  
Cancer Progression ◽  
Squamous Cell ◽  
Epithelial To Mesenchymal Transition ◽  
Squamous Cell Carcinomas ◽  
Epithelial Tissue ◽  
Mesenchymal Transition ◽  
Invasion Front ◽  
Knowing That ◽  
Tumoral Cells ◽  
E Cadherin

E-cadherin is an adhesion molecule essential in maintaining cellular integrity and preserving normal epithelial tissue architecture in adult organisms. Loss of E-cadherin expression and epithelial characteristics has been described in the late stages of carcinogenesis in various human cancers. By loosing cell-cell adhesion mediated by E-cadherin and acquiring mesenchymal properties, a process reffered to as epithelial to mesenchymal transition (EMT), carcinoma cells become more motile and invasive, thus being able to penetrate the surrounding stroma. Our aim is to investigate E-cadherin expression, part of the EMT phenomenom, in cutaneous squamous cell carcinomas (cSCCs), knowing that it represents a valuable model for understanding cancer progression. We conducted a retrospective study, performing immunohistochemical staining of E-cadherin and analyzing its expression in 32 cases of primary cSCCs. E-cadherin membrane positivity was assessed in cells from the main tumor and cells from the invasion front and described in terms of percentage of positive tumoral cells and in terms of intensity. Statistycal analysis showed the proportion of E-Cadherin positive cells in the tumor central and superficial areas is lower in higher degrees of anaplasia (marginally significant p=0.07), confirming the higher potential of poor outcome in these tumors. Median intensity and proportion values of E-Cadherin positive cells were significantly higher in the tumor central and superficial areas than in the invasion front (p<0.0001), suggesting that loss of epithelial features portends higher potential of invasion and metastasis in the setting of EMT. Further studies are required in order to establish clear correlations.

scholarly journals Differences in E-Cadherin and Syndecan-1 Expression in Different Types of Ameloblastomas

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Ramón G. Carreón-Burciaga ◽  
Rogelio González-González ◽  
Nelly Molina-Frechero ◽  
Sandra López-Verdín ◽  
Vanesa Pereira-Prado ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Adhesion Molecules ◽  
Tumor Size ◽  
Cell Adhesion Molecules ◽  
Strong Association ◽  
Tumor Aggressiveness ◽  
Future Studies ◽  
Unicystic Ameloblastoma ◽  
Different Types ◽  
E Cadherin

Ameloblastomas are a group of benign, locally aggressive, recurrent tumors characterized by their slow and infiltrative growth. E-Cadherin and syndecan-1 are cell adhesion molecules related to the behavior of various tumors, including ameloblastomas. Ninety-nine ameloblastoma samples were studied; the expression of E-cadherin and syndecan-1 were evaluated by immunohistochemistry. E-Cadherin and epithelial syndecan-1 were more highly expressed in intraluminal/luminal unicystic ameloblastoma than in mural unicystic ameloblastoma and solid/multicystic ameloblastoma, whereas the stromal expression of syndecan-1 was higher in mural unicystic ameloblastoma and solid/multicystic ameloblastoma. Synchronicity was observed between E-cadherin and epithelial syndecan-1; the expression was correlated with intensity in all cases. There was a strong association between expression and tumor size and recurrence. The evaluation of the expression of E-cadherin and syndecan-1 are important for determining the potential aggressiveness of ameloblastoma variants. Future studies are required to understand how the expression of these markers is related to tumor aggressiveness.

scholarly journals Ultrastructural localization of E-cadherin cell adhesion molecule on the cytoplasmic membrane of keratinocytes in vivo and in vitro.

1994 ◽  
Vol 42 (10) ◽  
pp. 1333-1340 ◽  
Author(s):  
Y Horiguchi ◽  
F Furukawa ◽  
M Fujita ◽  
S Imamura
Keyword(s):  
Cell Adhesion ◽  
Free Surface ◽  
Adhesion Molecules ◽  
Cell Adhesion Molecules ◽  
Cytoplasmic Membrane ◽  
Ultrastructural Localization ◽  
In Vivo Studies ◽  
E Cadherin

We examined the ultrastructural localization of E (epithelial)-cadherin cell adhesion molecules by immunoperoxidase electron microscopy on the epithelium of mouse intestine, epidermis of human skin, and cultured human keratinocytes. The in vivo studies demonstrated that E-cadherin was present at the intermediate junction but not at the desmosome of the mouse intestinal single epithelium, and was found on the cytoplasmic membranes of keratinocytes with condensation in the intercellular space of the desmosomes, except for the basal surface of the basal cells. In vitro studies demonstrated that keratinocytes cultured in medium containing a low Ca2+ concentration (0.1 mM) lacked the tight connection through desmosomes, and that E-cadherin showed diffuse distribution and dot-like accumulation around the free surface of the cytoplasmic membrane. In culture medium containing a high concentration of Ca2+ (0.6 mM), keratinocytes formed desmosomal adhesion structures in which E-cadherin was accumulated. The free surface of the keratinocytes in this medium showed weaker distribution and a lesser amount of dot-like accumulation of E-cadherin than that in a low Ca2+ condition. These findings suggest that the distribution pattern of the E-cadherin cell adhesion molecules on the keratinocytes is different from that on the single epithelium of the intestine, and that E-cadherin on the cytoplasmic membrane of the keratinocytes shifts to the desmosomes under physiological conditions, participating in adhesion in association with other desmosomal cadherins.

scholarly journals The Role of Immunoglobulin Superfamily Cell Adhesion Molecules in Cancer Metastasis

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Chee Wai Wong ◽  
Danielle E. Dye ◽  
Deirdre R. Coombe
Keyword(s):  
Cell Adhesion ◽  
Adhesion Molecules ◽  
Cancer Progression ◽  
Cell Adhesion Molecules ◽  
Cancer Metastasis ◽  
Clinical Problem ◽  
Metastatic Lesion ◽  
Immunoglobulin Superfamily ◽  
Metastatic Pathway ◽  
Cell Cell

Metastasis is a major clinical problem and results in a poor prognosis for most cancers. The metastatic pathway describes the process by which cancer cells give rise to a metastatic lesion in a new tissue or organ. It consists of interconnecting steps all of which must be successfully completed to result in a metastasis. Cell-cell adhesion is a key aspect of many of these steps. Adhesion molecules belonging to the immunoglobulin superfamily (Ig-SF) commonly play a central role in cell-cell adhesion, and a number of these molecules have been associated with cancer progression and a metastatic phenotype. Surprisingly, the contribution of Ig-SF members to metastasis has not received the attention afforded other cell adhesion molecules (CAMs) such as the integrins. Here we examine the steps in the metastatic pathway focusing on how the Ig-SF members, melanoma cell adhesion molecule (MCAM), L1CAM, neural CAM (NCAM), leukocyte CAM (ALCAM), intercellular CAM-1 (ICAM-1) and platelet endothelial CAM-1 (PECAM-1) could play a role. Although much remains to be understood, this review aims to raise the profile of Ig-SF members in metastasis formation and prompt further research that could lead to useful clinical outcomes.

Attenuated expression of epithelial cell adhesion molecules in murine polycystic kidney disease

1992 ◽  
Vol 262 (4) ◽  
pp. F679-F686 ◽  
Author(s):  
M. V. Rocco ◽  
E. G. Neilson ◽  
J. R. Hoyer ◽  
F. N. Ziyadeh
Keyword(s):  
Cell Adhesion ◽  
Growth Factors ◽  
Kidney Disease ◽  
Adhesion Molecules ◽  
Polycystic Kidney Disease ◽  
Cell Adhesion Molecules ◽  
Structural Proteins ◽  
Polycystic Kidney ◽  
Cystic Kidneys ◽  
E Cadherin

Polycystic kidney disease is an inherited disorder of parenchymal structure that leads to renal failure. Cysts begin as focal dilations in proximal tubules and collecting ducts, giving rise to cyst walls lined by a phenotypically disturbed epithelium that expresses dysfunctional transport and matrix proteins. We used an mRNA search protocol to probe efficiently for tissue-specific disturbances that might underlie the formation of cysts. This search assessed the relative abundance of transcripts encoding a variety of growth factors (transforming growth factor-beta 1, interleukin-6, tumor necrosis factor, and endothelin-1), structural proteins (collagen IV, nidogen, fibronectin, and laminins A and B1), and cell adhesion molecules (CAMs; E-cadherin, N-CAM, laminin receptor, and fibronectin receptor) in the cystic kidneys of cpk/cpk mice and uncovered a previously unrecognized early reduction in mRNA encoding N-CAM (54%) and E-cadherin (56%) (n = 5; P less than 0.001). Levels of transcripts for growth factors, structural proteins, and for fibronectin and laminin receptors in normal and cystic kidneys were generally similar. The reduction in transcripts for N-CAM and E-cadherin in kidneys from cystic mice was not observed in autologous liver. The immunofluorescent staining of cystic kidneys confirmed that the decrease in N-CAM and E-cadherin was generally confined to regions abundant in developing cystic epithelium. The presence of both N-CAM and E-cadherin appears to guide the sequential differentiation and polarization of normal renal epithelium, and their attenuated expression in the kidney of cpk/cpk mice may be a material factor contributing to the pathogenesis of cyst formation.

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