Dysregulated Expression of Tensin ۲ and Components of the PI۳ Kinase/Akt Signaling Pathway in Human Thyroid Carcinoma

Background: The phosphatidylinositol ۳-kinase/Akt signaling pathway is recognized as a key driver of cancer cell survival and proliferation, and is often contingent upon an impairment of expression/function of the PTEN tumor suppressor, a negative regulator of this pathway. In addition, the cytoskeletal signaling protein Tensin ۲ has also been implicated as a negative regulator of this pathway. However, the PI۳K pathway remains to be fully characterized in clinical thyroid carcinomas. The aim of this study is to determine the expression of components of the PI۳K pathway in neoplastic and normal tissue sections obtained from patients with thyroid carcinoma.Methods: Tissues from ۵۸ cases with thyroid carcinoma underwent immunohistochemistry for activated Akt (phosphorylated Akt, pAkt), Tensin ۲ and PTEN.Results: A total of ۱۰۰% of thyroid cancerous tissues were positive for pAkt staining compared to ۶۷.۹% of normal tissues. In contrast, ۴۶.۸% of cancer tissues were positive for Tensin ۲ compared to ۶۱.۷% of normal tissues. For PTEN, ۸۲.۸% of cancerous tissues and ۶۷.۲% of normal tissues stained positive for this protein. There were no associations between the expression levels of the molecules with the patients’ clinicopathological characteristics.Conclusion:We have found evidence for an enhanced activation of the PI۳K/Akt signaling pathway in clinical thyroid carcinoma tissues. This can be coupled with concomitant downregulation of Tensin ۲. Further work is required to determine the relative significance of PTEN expression versus its activity in thyroid carcinoma in order to determine its role in the observed increased Akt activity.