Roles of caveolin-1 on anoikis resistance in non small cell lung cancer

Abstract

Advance therapies which effectively reduce mortality in lung cancer patients become a global health challenge nowadays. Sufficient knowledge regarding cellular and molecular basis of cancer progression and metastasis would possibly help in the development of novel and effective strategies for the treatment of this disease. This review focuses on the information regarding the role and mechanism of caveolin-1 (Cav-1) protein on anoikis in Non Small Cell Lung Cancer (NSCLC). NSCLC accounts of approximately 80% of all diagnosed lung cancer cases which patients frequently presented with metastatic disease. Like other cancers, caveolin-1 (Cav-1) has been shown to play an important role in regulating cancer-cells behaviors including apoptosis resistance and metastasis. Even though further investigations as well as in vivo experiments are required, these data are of great interest and may be beneficial to the development of lung cancer therapy.

Keywords: Caveolin-1 (Cav-1); Non Small Cell Lung Cancer (NSCLC); anoikis resistance; apoptosis resistance; cancer therapy; metastasis.

Figure 1

The scheme representing effects of reactive oxygen species and nitric oxide in regulation of cancer cell anoikis through a caveolin-1-dependent pathway. In the attached condition, hydroxyl radical enhances cancer cell migration and invasion by increasing the level of caveolin-1 protein, while hydrogen peroxide and superoxide anion play an opposite effect. Under cell detachment condition, the loss of cell-extracellular matrix interaction mediates caveolin-1 down-regulation and anoikis. Endogenous hydrogen peroxide functions in maintaining caveolin-1 level which subsequently suppressed anoikis. Also, exogenous hydrogen peroxide and nitric oxide sustains such caveolin-1 level and inhibited anoikis response of the cells. During anoikis, caveolin-1 inhibits anoikis via Mcl-1 and/or Akt-dependent pathways.