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PI3K/AKT Pathway and Its Mediators in Thyroid Carcinomas
Zahra Nozhat1,2, Mehdi Hedayati3
1Cellular and Molecular Endocrine Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Molecular Diagnosis & Therapy
|November 25, 2015
Summary
Thyroid cancer involves the PI3K-PKB/AKT pathway, crucial for cell growth. Targeting this pathway, particularly mTOR, shows promise, with future strategies exploring FOXOs and PTEN for enhanced treatment.
Area of Science:
- Endocrinology
- Oncology
- Molecular Biology
Background:
- Thyroid malignancies are common endocrine carcinomas with diverse histopathology.
- The phosphoinositide 3-kinase-protein kinase B/AKT (PI3K-PKB/AKT) pathway is vital in cellular processes and frequently dysregulated in cancers.
- Aberrant PI3K-PKB/AKT signaling drives cell proliferation in various cancers, including thyroid carcinomas.
Purpose of the Study:
- To review the role of PI3K/AKT signaling pathways in thyroid cancers.
- To emphasize the PI3K/AKT/mammalian target of rapamycin (mTOR), PI3K/AKT/forkhead box O (FOXO), and PI3K/AKT/phosphatase and tensin homolog deleted on chromosome ten (PTEN) pathways.
- To summarize therapeutic strategies targeting these pathways in thyroid cancer.
Main Methods:
- Literature review of signaling pathways in thyroid cancer.
- Analysis of in vitro studies on therapeutic agents.
- Exploration of downstream targets like mTOR, FOXOs, and PTEN.
Main Results:
- Inhibitors of mTOR show promise as monotherapy or in combination with chemotherapy for thyroid malignancies.
- FOXO and PTEN are key downstream targets of the PI3K/AKT pathway.
- No current studies focus on thyroid cancer treatment targeting FOXOs and PTEN.
Conclusions:
- Targeting the PI3K/AKT pathway, especially mTOR, offers promising therapeutic strategies for thyroid cancer.
- Inducing FOXOs or PTEN activity, combined with inhibition of PI3K/AKT downstream mediators like mTOR, may represent a beneficial future treatment approach for thyroid cancer.
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