Synergistic effects of thyroid hormone receptor beta with selective agonist GC-1 and bromodomain inhibitors in ATC
Abstract
Anaplastic thyroid cancer (ATC) is the fastest-growing cancer worldwide, with no treatment. ATC typically has an abnormal chromatin environment that alters gene expression. Thyroid hormone receptor beta (TRß) is a nuclear transcription factor and an ATC tumor suppressor. TRß activates bromodomain-containing proteins (BRDs), which open and close DNA to transcriptional machinery. The altered DNA structures mollify the cancer. Amplifying the effect of TRß on BRDs should suppress ATC powerfully. Our research will quantify the impact of select bromodomain inhibitors on an aggressive thyroid cancer phenotype. We will determine if the bromodomain inhibitors work synergistically with TRß agonism to combat ATC.
Primary Faculty Mentor Name
John Barlow
Status
Graduate
Student College
College of Agriculture and Life Sciences
Program/Major
Biochemistry
Primary Research Category
Life Sciences
Synergistic effects of thyroid hormone receptor beta with selective agonist GC-1 and bromodomain inhibitors in ATC
Anaplastic thyroid cancer (ATC) is the fastest-growing cancer worldwide, with no treatment. ATC typically has an abnormal chromatin environment that alters gene expression. Thyroid hormone receptor beta (TRß) is a nuclear transcription factor and an ATC tumor suppressor. TRß activates bromodomain-containing proteins (BRDs), which open and close DNA to transcriptional machinery. The altered DNA structures mollify the cancer. Amplifying the effect of TRß on BRDs should suppress ATC powerfully. Our research will quantify the impact of select bromodomain inhibitors on an aggressive thyroid cancer phenotype. We will determine if the bromodomain inhibitors work synergistically with TRß agonism to combat ATC.
