Dysregulated expression of Tensin2 and components of the PI3 Kinase/Akt signaling pathway in human thyroid carcinoma

Background: The phosphatidylinositol 3-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 Tensin2 has also been implicated as a negative regulator of this pathway. However, the PI3K pathway remains to be fully characterized in clinical thyroid carcinomas. The aim of this study is to determine the expression of components of the PI3K pathway in neoplastic and normal tissue sections obtained from patients with thyroid carcinoma.

Methods: Tissues from 58 cases with thyroid carcinoma underwent immunohistochemistry for activated Akt (phosphorylated Akt, pAkt), Tensin2 and PTEN.

Results: A total of 100% of thyroid cancerous tissues were positive for pAktstaining compared to 67.9% of normal tissues. In contrast, 46.8% of cancer tissues werepositive for Tensin2 compared to 61.7% of normal tissues. For PTEN, 82.8% ofcancerous tissues and 67.2% 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 PI3K/Aktsignaling pathway in clinical thyroid carcinoma tissues. This can be coupled withconcomitant downregulation of Tensin2. 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.