Presenter's Name(s)

Cole DavidsonFollow

Primary Faculty Mentor Name

Frances Carr

Status

Graduate

Student College

Larner College of Medicine

Program/Major

Cellular, Molecular and Biomedical Sciences

Primary Research Category

Biological Sciences

Presentation Title

Thyroid Hormone Receptor Beta Suppresses PI3K and Metabolic Signaling in Thyroid Cancer

Time

11:00 AM

Location

Silver Maple Ballroom - Biological Sciences

Abstract

Thyroid cancer is the most common endocrine malignancy, and the rate has been increasing over the past few decades. A commonly unregulated pathway in poorly differentiated thyroid cancer is PI3K signaling. This pathway ends in the activation of translation factors necessary for anabolism, cell growth, and division. However, reintroduction of thyroid hormone receptor beta (TRß) and thyroid hormone (T3) application reduces PI3K activity via TRß binding to the regulatory subunit of PI3K. Furthermore, the TRß residue, Y406 is necessary for this binding as PI3K suppression is lost with the phosphomutant, Y406F. PI3K signaling results in the increased expression of key metabolic proteins seen in anaplastic thyroid cancer (ATC). Novel phenotypic studies were conducted that show a decreased oxidative phosphorylation profile but increased glycolysis rate and glutamine metabolism in ATC. Taken together, these results suggest an application of thyroid hormone and receptor for suppressing PI3K and metabolic signaling in ATC.

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Thyroid Hormone Receptor Beta Suppresses PI3K and Metabolic Signaling in Thyroid Cancer

Thyroid cancer is the most common endocrine malignancy, and the rate has been increasing over the past few decades. A commonly unregulated pathway in poorly differentiated thyroid cancer is PI3K signaling. This pathway ends in the activation of translation factors necessary for anabolism, cell growth, and division. However, reintroduction of thyroid hormone receptor beta (TRß) and thyroid hormone (T3) application reduces PI3K activity via TRß binding to the regulatory subunit of PI3K. Furthermore, the TRß residue, Y406 is necessary for this binding as PI3K suppression is lost with the phosphomutant, Y406F. PI3K signaling results in the increased expression of key metabolic proteins seen in anaplastic thyroid cancer (ATC). Novel phenotypic studies were conducted that show a decreased oxidative phosphorylation profile but increased glycolysis rate and glutamine metabolism in ATC. Taken together, these results suggest an application of thyroid hormone and receptor for suppressing PI3K and metabolic signaling in ATC.