Loss of α1β1 and reduced expression of other β1 integrins and cam in lung adenocarcinoma compared with pneumocytes

Eugène Roussel, Marie‐Claude ‐C Gingras, Jae Y. Ro, Cynthia Branch, Jack A. Roth

Research output: Contribution to journalArticlepeer-review

28 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)198-208
Number of pages11
JournalJournal of Surgical Oncology
Issue number3
StatePublished - Jul 1994


  • cell adhesion molecules
  • endothelium
  • image analysis
  • immunohistochemistry
  • integrins
  • lung tumor

ASJC Scopus subject areas

  • Surgery
  • Oncology


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