scholarly journals AnnexinA7 and CAP1 are associated with regulating tumor cell adhesion molecule expression and biological behavior

2021 ◽  
Author(s):  
Li Wang ◽  
Yang Wang ◽  
Zhiyan Liu ◽  
Yixia Zhou ◽  
Jun Zhang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Adhesion ◽  
Lymph Node ◽  
Adhesion Molecules ◽  
Biological Behavior ◽  
Tumor Cell Adhesion ◽  
Protein Levels ◽  
The Relationship ◽  
P Cells ◽  
E Cadherin

IntroductionTo find out the correlations between the effects of down-regulating AnnexinA7 and CAP1 gene on cell adhesion factors and the biological behavior of Hca-p cells cells, and finally infer the relationship between the two genes.Material and methodsWestern blot ,qRT-PCR,immunocytochemistry, CCK8 cell proliferation, flow cytometry, lymph node adhesion and transwell chamber assay testing .ResultsAnnexinA7 and CAP1 were consistent with the regulation of the expression of the adhesion molecules such as FAK, Src, Paxillin and E-cadherin. At the mRNA and protein levels, the expression of FAK, Src and Paxillin were increased with down-regulated AnnexinA7 and CAP1 genes, while E-cadherin was down-regulated in the change of these two genes. And the low expression of AnnexinA7 could affect the expression of CAP1 in mRNA and protein levels. otherwise, the localization of AnnexinA7 and CAP1 in hepatocellular carcinoma cells was also the same. After down-regulating the expression of CAP1, the functions of proliferation, lymph node adhesion and invasion were increased and early apoptotic ability was decreased in Hca-P cells.ConclusionsAnnexinA7 and CAP1 could control the expression of these adhesion molecules in the same trend. We speculated they may be co-localization. And AnnexinA7 gene may be related to the molecular mechanism of CAP1 gene, which is likely to have a consistent effect on cell adhesion molecules and be closely related to the biological behaviors of Hca-P cells.AnnexinA7 and CAP1 may play an inhibitory role in lymph node metastasis to provide a reliable basis for the early identification of lymphatic metastasis in hepatocellular carcinoma.

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 Evaluation of the expression of integrins and cell adhesion molecules through tissue microarray in lymph node metastases of prostate cancer

2009 ◽  
Vol 8 (1) ◽  
pp. 3 ◽  
Author(s):  
Jose Pontes-Junior ◽  
SabrinaThalita Reis ◽  
Marcos Dall′Oglio ◽  
LuisCarlos Neves de Oliveira ◽  
Jose Cury ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Adhesion ◽  
Lymph Node ◽  
Adhesion Molecules ◽  
Tissue Microarray ◽  
Lymph Node Metastases ◽  
Cell Adhesion Molecules ◽  
Node Metastases

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.

scholarly journals Aberrant cell adhesion molecule expression in human bronchopulmonary sequestration and congenital cystic adenomatoid malformation

2009 ◽  
Vol 297 (1) ◽  
pp. L143-L152 ◽  
Author(s):  
MaryAnn V. Volpe ◽  
Eunice Chung ◽  
Jason P. Ulm ◽  
Brian F. Gilchrist ◽  
Steven Ralston ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Human Lung ◽  
Congenital Cystic Adenomatoid Malformation ◽  
Adhesion Molecule Expression ◽  
Protein Levels ◽  
Normal Human ◽  
Hox Protein ◽  
E Cadherin

In many organs, integrins and cadherins are partly regulated by Hox genes, but their interactions in airway morphogenesis and congenital lung diseases are unknown. We previously showed that the Hox protein HoxB5 is abnormally increased in bronchopulmonary sequestration (BPS) and congenital cystic adenomatoid malformation (CCAM), congenital lung lesions with abnormal airway branching. We now report on α2-, α3-, and β1-integrin and E-cadherin expression in normal human lung and in BPS and CCAM tissue previously shown to have abnormal HoxB5 expression and on the relationship of cell adhesion molecule expression to Hoxb5 regulation. α2-, α3-, and β1-integrins and E-cadherin expression in normal human lung and BPS and CCAM were evaluated using Western blot and immunohistochemistry. Fetal mouse lung fibroblasts with Hoxb5-specific siRNA downregulation were evaluated for α2-integrin protein levels by Western blot. Compared with normal human lung, a previously undetected α2-integrin isoform potentially lacking essential cytoplasmic sequences was significantly increased in BPS and CCAM, and α2-integrin spatial and cellular expression was more intense. E-cadherin protein levels were also significantly increased, whereas α3 increased in CCAM compared with canalicular, but not with alveolar, stage lung. β1-integrin levels were unchanged. We conclude that in BPS and CCAM, altered α2-integrin cytoplasmic signaling contributes to abnormal cellular behavior in these lung lesions. Aberrant cell adhesion molecule and Hox protein regulation are likely part of the mechanism involved in the development of BPS and CCAM.

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