retinamide and Glioma

The present study was performed to investigate the effect of retinoic acid amide (RAA) on the expression of integrin α3β1, rate of cell proliferation and migration in p53-deficient glioma cell line, LN-308. The results revealed promotion of integrin α3 expression, reduction in proliferation and migration in RAA treated cells compared to the control LN-308 glioma cells. Promotion of RAA induced integrin α3β1 expression led to the enhancement in cyclin-dependent kinase nuclear localization and activation of Akt pathway. In addition, RAA treatment inhibited the expression of nuclear factor-κB, Bcl-2 and epidermal growth factor receptor (EGFR). These factors are responsible for promoting the rate of cell proliferation and survival in the carcinoma cells. Thus RAA treatment inhibits rate of LN-308 glioma cell proliferation and migration through increase in integrin α3β1 expression and activation of Akt pathway. Therefore, RAA can be of therapeutic importance for the treatment of glioma.

Topics: Antineoplastic Agents; Brain Neoplasms; Cell Cycle Proteins; Cell Line, Tumor; Cell Movement; Cell Proliferation; Enzyme Activation; ErbB Receptors; Gene Expression Regulation, Neoplastic; Glioma; Humans; Integrin alpha3beta1; Neoplasm Invasiveness; NF-kappa B; Protein Kinase Inhibitors; Proto-Oncogene Proteins c-akt; Proto-Oncogene Proteins c-bcl-2; RNA Interference; Signal Transduction; Time Factors; Transfection; Tretinoin