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Updated: Jun 5, 2026

Induction and Analysis of Epithelial to Mesenchymal Transition
Published on: August 27, 2013
Contribution of PKB/AKT signaling to thyroid cancer
Giuseppe Viglietto1, Nicola Amodio, Donatella Malanga
1Department of Experimental and Clinical Medicine, Magna Graecia University of Catanzaro, University Campus Germaneto, Catanzaro 88100, Italy. viglietto@unicz.it
Abstract:
The family of serine/threonine kinases B/Akt (hereafter Akt) represents a central node in signalling pathways downstream of growth factors, cytokines, and other cellular stimuli. In mammalian cells the Akt family comprises three highly homologous members -known as Akt1/PKBalpha, Akt2/PKBbeta, and Akt3/PKBgamma- that regulate several processes including cell proliferation and survival, growth and response to nutrient availability, migration, tissue invasion and angiogenesis. Aberrant activation of Akt is involved in a variety of human cancers including those arising in the thyroid gland. Here, we review the contribution of Akt-dependent pathway in the proliferation of normal thyrocytes, the different pathogenic mechanisms underlying aberrant Akt signalling in thyroid malignancies as well as the relative roles of Akt substrates that most likely contribute to the onset and/or progression of thyroid cancer. Finally, we discuss the current therapeutic strategies targeting the components of the PI3K/Akt pathway in the context of thyroid malignancy.
Insights
The Akt signaling pathway is crucial for cell growth and survival, and its abnormal activation contributes to thyroid cancer development. This review explores Akt
Area of Science:
- Molecular Biology
- Oncology
- Cell Signaling
Background:
- The Akt (also known as Protein Kinase B or PKB) serine/threonine kinase family is a central signaling node activated by growth factors and cytokines.
- Akt regulates fundamental cellular processes, including proliferation, survival, growth, nutrient response, migration, invasion, and angiogenesis.
- Aberrant Akt activation is implicated in various human cancers, notably thyroid malignancies.
Purpose of the Study:
- To review the role of the Akt pathway in normal thyrocyte proliferation.
- To elucidate pathogenic mechanisms of aberrant Akt signaling in thyroid cancer.
- To examine the contribution of Akt substrates to thyroid cancer onset and progression.
- To discuss current therapeutic strategies targeting the PI3K/Akt pathway in thyroid cancer.
Main Methods:
- Literature review and synthesis of existing research on Akt signaling in thyroid biology and cancer.
- Analysis of molecular mechanisms underlying Akt pathway dysregulation in thyroid malignancies.
- Evaluation of the roles of specific Akt substrates in thyroid cancer pathogenesis.
- Discussion of preclinical and clinical data on PI3K/Akt inhibitors for thyroid cancer treatment.
Main Results:
- The Akt pathway significantly influences normal thyrocyte proliferation.
- Various mechanisms lead to aberrant Akt signaling in thyroid tumors, promoting cancer development.
- Specific Akt substrates are identified as key contributors to thyroid cancer initiation and progression.
- Targeting the PI3K/Akt pathway represents a promising therapeutic avenue for thyroid cancer.
Conclusions:
- The Akt pathway is a critical regulator of thyroid cell function and a key driver of thyroid cancer.
- Understanding the specific Akt substrates and dysregulation mechanisms is essential for targeted therapy development.
- Targeting the PI3K/Akt pathway holds significant therapeutic potential for managing thyroid malignancies.
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