Integrin receptors in primary lung cancer (Journal article)

Gogali, A./ Charalabopoulos, K./ Constantopoulos, S.

In the present review recent data regarding the role of integrins--an important category of adhesion molecules mediating interactions among cells and components of the extracellular matrix--in lung cancer development is discussed. Investigations have shown that down-regulation of alpha3 integrin subunit may contribute to enhanced tumorigenicity of c-myc-overexpressing small cell lung carcinoma, while the loss of an integrin expression is correlated with recurrence in node-negative lung carcinoma. Increased expression of alpha1beta1 and alpha2beta1 integrins have been shown to be positively correlated with increased metastatic ability in squamous cell carcinoma. alpha3beta1 integrin is a most critical integrin for pulmonary development and epithelium integrity and its reduced expression in small cell lung cancer is probably related to the increased aggressiveness of this type. Pulmonary cancer cells generally express fewer integrin receptors than the normal epithelium. Additionally, since the ability of malignant cells to interact with extracellular matrix components is thought to be important, integrin dependent migration of lung cancer cells is a crucial process.
Institution and School/Department of submitter: Πανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικής
Keywords: Animals,Cell Adhesion,Cell Adhesion Molecules/metabolism,Humans,Integrins/genetics/immunology/*metabolism,Lung Neoplasms/*metabolism/pathology,Proto-Oncogene Proteins c-myc/metabolism
URI: https://olympias.lib.uoi.gr/jspui/handle/123456789/20725
ISSN: 1812-9269
Link: http://www.ncbi.nlm.nih.gov/pubmed/15273661
Appears in Collections:Άρθρα σε επιστημονικά περιοδικά ( Ανοικτά)

Files in This Item:
There are no files associated with this item.


 Please use this identifier to cite or link to this item:
https://olympias.lib.uoi.gr/jspui/handle/123456789/20725
  This item is a favorite for 0 people.

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.