TY - JOUR
T1 - Loss of α1β1 and reduced expression of other β1 integrins and cam in lung adenocarcinoma compared with pneumocytes
AU - Roussel, Eugène
AU - Gingras, Marie‐Claude ‐C
AU - Ro, Jae Y.
AU - Branch, Cynthia
AU - Roth, Jack A.
N1 - Copyright:
Copyright 2016 Elsevier B.V., All rights reserved.
PY - 1994/7
Y1 - 1994/7
N2 - Alterations in expression of various cell-adhesion molecules have been reported in a variety of malignant tissues. However, little is known about how lung adenocarcinomas differ in CAM expression from the normal lung. We analyzed the expression of integrins α1β1 through α6β1, intercellular adhesion molecule (ICAM)-1, neural cell adhesion molecule (NCAM), and lymphocyte function antigen (LFA)-3, CD44, and the two carbohydrate antigens. Lewis(x) (Le(x)) and sialosyl-Le-Le(x) of lung adenocarcinoma cells, and compared them with autologous pneumocytes. CAM expression was studied by an immunohistochemical method using monoclonal antibodies, and computerized image analysis was used to quantify the immunoperoxidase-staining intensity. The normal lung alveolar cells strongly expressed the integrins α1β1 and α3β1, and fairly expressed α2β1, α4β1, α5β1, and α6β1. ICAM-1, LFA-3, and CD44 were strongly expressed, whereas NCAM, the Le(x) and sialosyl-Le-Le(x) antigens, were expressed weakly. In contrast, we did not detect expression of the α1β1 integrin on any autologous lung adenocarcinoma cells, and they showed on average a 50% reduction in labeling relative intensity units for the integrin common chain marker β1, the specific integrins α3β1, α5β1, and α6β1, and ICAM-1, and LFA-3. Examination of the adjacent small blood vessel endothelium in malignant lung tissues did not reveal any major alterations in CAM expression, the small vessel endothelium of the normal and malignant lung tissues appeared with a similar CAM profile. These results suggest that lung adenocarcinoma cells have a lack of α1β1 expression and significant reduction in some other integrin β1 and CAM expression in comparison with their autologous pneumocytes. This aberration in CAM expression by the lung adenocarcinoma cells may be involved in their loss of proliferation control and may interfere with leukocyte adhesion to tumor cells, enabling the tumor to escape immunodestruction.
AB - Alterations in expression of various cell-adhesion molecules have been reported in a variety of malignant tissues. However, little is known about how lung adenocarcinomas differ in CAM expression from the normal lung. We analyzed the expression of integrins α1β1 through α6β1, intercellular adhesion molecule (ICAM)-1, neural cell adhesion molecule (NCAM), and lymphocyte function antigen (LFA)-3, CD44, and the two carbohydrate antigens. Lewis(x) (Le(x)) and sialosyl-Le-Le(x) of lung adenocarcinoma cells, and compared them with autologous pneumocytes. CAM expression was studied by an immunohistochemical method using monoclonal antibodies, and computerized image analysis was used to quantify the immunoperoxidase-staining intensity. The normal lung alveolar cells strongly expressed the integrins α1β1 and α3β1, and fairly expressed α2β1, α4β1, α5β1, and α6β1. ICAM-1, LFA-3, and CD44 were strongly expressed, whereas NCAM, the Le(x) and sialosyl-Le-Le(x) antigens, were expressed weakly. In contrast, we did not detect expression of the α1β1 integrin on any autologous lung adenocarcinoma cells, and they showed on average a 50% reduction in labeling relative intensity units for the integrin common chain marker β1, the specific integrins α3β1, α5β1, and α6β1, and ICAM-1, and LFA-3. Examination of the adjacent small blood vessel endothelium in malignant lung tissues did not reveal any major alterations in CAM expression, the small vessel endothelium of the normal and malignant lung tissues appeared with a similar CAM profile. These results suggest that lung adenocarcinoma cells have a lack of α1β1 expression and significant reduction in some other integrin β1 and CAM expression in comparison with their autologous pneumocytes. This aberration in CAM expression by the lung adenocarcinoma cells may be involved in their loss of proliferation control and may interfere with leukocyte adhesion to tumor cells, enabling the tumor to escape immunodestruction.
KW - cell adhesion molecules
KW - endothelium
KW - image analysis
KW - immunohistochemistry
KW - integrins
KW - lung tumor
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U2 - 10.1002/jso.2930560315
DO - 10.1002/jso.2930560315
M3 - Article
C2 - 7518021
AN - SCOPUS:0028290407
VL - 56
SP - 198
EP - 208
JO - Journal of Surgical Oncology
JF - Journal of Surgical Oncology
SN - 0022-4790
IS - 3
ER -