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A number of studies have indicated that thyroid hormone receptor β1 (TRβ1) functions as a tumor suppressor. TRs mediate transcriptional responses through a highly conserved DNA-binding domain (DBD). A novel rat TRβ isoform (rTRβΔ) was previously identified, in which a novel exon, N (108 bp), is located between exons 3 and 4 within the DBD; this exon represents the only difference between rTRβΔ and rTRβ1. In vitro , rTRβΔ exhibits a stronger tumor-suppressive capacity than rTRβ1, and further analysis revealed a high level of conservation between the rat and human DBD sequences. In the present study, an artificially modified human TRβ1 (m-hTRβ1) was constructed via the introduction of the 108-bp sequence into the corresponding position of the wild-type human TRβ1 (wt-hTRβ1) DBD. An electrophoretic mobility shift assay and transfection experiments confirmed that m-hTRβ1 is functional. Overexpression of m-hTRβ1 inhibits the proliferation of MDA-MB-468 cells in the presence of triiodothyronine by promoting apoptosis, which may be associated with the upregulation of Caspase-3 and Bak gene expression and the activation of the Caspase-3 protein. In addition, the pro-apoptotic effect of m-hTRβ1 was stronger, compared with wt-hTRβ1. These results indicated that m-hTRβ1 may act as a tumor suppressor in MDA-MB-468 cells. These data provided a novel insight into gene therapy for breast cancer.

Overexpressing modified human TRβ1 suppresses the proliferation of breast cancer MDA‑MB‑468 cells