Effect of Thyroid Hormone Receptor βΔ on Proliferation and Apoptosis of Rat Breast Cancer Cells SHZ-88

Objective To investigate the effect of thyroid hormone receptor βΔ(TRβΔ) on the proliferation and apoptosis of rat breast cancer cell line SHZ-88 in vitro and related mechanism.

Methods The expression plasmid pcDNA3.1-TrβΔ and empty vector pcDNA3.1 were compared in the presence or absence of 10 nmol/L T3. Cell Counting Kit-8 was used to measure SHZ-88 cells activity. The apoptotic rate and mitochondrial transmembrane potential were analyzed by flow cytometry. Histone/DNA fragment was assayed by ELISA. The levels of Cysteinyl aspartate specific proteinase-9(Caspase-9), Caspase-3 mRNA were detected by quantitative RT-qPCR. The activity of Caspase-9 and caspase-3 were measured using colorimetry.

Results Compared with empty vector pcDNA3.1 transfection group, pcDNA3.1-TrβΔ transfection group significantly inhibited the cell proliferation, increased the level of histone/DNA fragment and the percentage of apoptotic cells, up-regulated Caspase-9, Caspase-3 expression and activity, and reduced the mitochondrial transmembrane potential in SHZ-88 cells(P<0.05). These effects could be significantly strengthened by T3(P<0.05).

Conclusion TRβΔ could inhibit the proliferation of SHZ-88 cells and enhance cell apoptosis, which might be via reducing the mitochondrial transmembrane potential, activating Caspase-9 and Caspase-3 protein, and starting endogenous apoptotic pathway, moreover, these effect could be regulated by T3.