Preprint Review Version 1 Preserved in Portico This version is not peer-reviewed

Thyroid Hormone Receptor Beta as Tumor Suppressor: Untapped Potential in Treatment and Diagnostics in Solid Tumors

Version 1 : Received: 22 July 2021 / Approved: 23 July 2021 / Online: 23 July 2021 (15:14:12 CEST)

A peer-reviewed article of this Preprint also exists.

Davidson, C.D.; Gillis, N.E.; Carr, F.E. Thyroid Hormone Receptor Beta as Tumor Suppressor: Untapped Potential in Treatment and Diagnostics in Solid Tumors. Cancers 2021, 13, 4254. Davidson, C.D.; Gillis, N.E.; Carr, F.E. Thyroid Hormone Receptor Beta as Tumor Suppressor: Untapped Potential in Treatment and Diagnostics in Solid Tumors. Cancers 2021, 13, 4254.

Journal reference: Cancers 2021, 13, 4254
DOI: 10.3390/cancers13174254

Abstract

There is compelling evidence that the nuclear receptor TRβ, a member of the thyroid hormone receptor (TR) family, is a tumor suppressor in thyroid, breast and other solid tumors. Cell-based and animal studies reveal that the liganded TRβ induces apoptosis, reduces an aggressive phenotype, decreases stem cell populations, and slows tumor growth through modulation of a complex interplay of transcriptional networks. TRβ-driven tumor suppressive transcriptomic signatures include repression of known drivers of proliferation such as PI3K/Akt pathway and activation of novel signaling (JAK1/STAT1) and metabolic reprogramming in both thyroid and breast cancers. The presence of TRβ is also correlated with a positive prognosis and response to therapeutics in BRCA+ and triple-negative breast cancers respectively. Ligand activation of TRβ enhances sensitivity to chemotherapeutics. TRβ co-regulators and bromodomain-containing chromatin remodeling proteins are emergent therapeutic targets. This review considers TRβ as a potential biomolecular diagnostic and therapeutic target.

Keywords

TRβ; tumor suppression; co-regulators; therapeutics

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