Akt, also known as protein kinase B, is a central signaling molecule in the phosphatidyl inositol 3-kinase (PI3K) pathway. Akt activation in response to growth factors or insulin plays important roles in the regulation of several cellular functions including nutrient metabolism, cell growth, apoptosis and survival. Enhanced activation of the Akt signaling pathway is frequently identified in human cancers. It has been suggested that in thyroid cancer, Akt activation is involved in tumorigenesis, particularly in both inherited and sporadic forms of follicular thyroid cancer. PI3K signaling pathway also appears to play an important role in progression of both papillary and follicular cancers.

The aim of this study was analysis of Akt1 kinase expression and subcellular distribution in benign and malignant thyroid neoplasms. The studies were performed on 6 specimens of follicular adenomas, 4- follicular carcinomas, 15- papillary carcinomas and 3- anaplastic carcinomas. Ten cases of non-neoplastic specimens were used as a control. The presence of Akt1 in cytoplasmic and nuclear fractions was analyzed by Western blot and enzyme-linked immunosorbent assay (ELISA). Akt1 presence was found both in cytoplasmic and nuclear fractions in all kinds of thyroid lesions. The level of cytoplasmic Akt1 from non-neoplastic lesions was significant lower than in tumor cases. Differences were noted in the subcellular distribution of Akt1 in anaplastic carcinomas versus the other tumors. Mainly cytoplasmic localization of Akt1 was detected in papillary and follicular carcinomas as well as adenomas. By contrast, nuclear localization was characteristic for the anaplastic thyroid cancers.

The results suggest that overexpression of Akt1 may play a role in the tumorigenesis of thyroid cancer. Nuclear localization and activation of Akt1 may be a late stage event .

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