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ZHANG Yangyang, PENG Xiaoxiang, SUN Yanli, SONG Wei, ZHAO Ronglan. Effect of Thyroid Hormone Receptor βΔ on Proliferation and Apoptosis of Rat Breast Cancer Cells SHZ-88[J]. Cancer Research on Prevention and Treatment, 2016, 43(12): 1018-1022. DOI: 10.3971/j.issn.1000-8578.2016.12.002
Citation: ZHANG Yangyang, PENG Xiaoxiang, SUN Yanli, SONG Wei, ZHAO Ronglan. Effect of Thyroid Hormone Receptor βΔ on Proliferation and Apoptosis of Rat Breast Cancer Cells SHZ-88[J]. Cancer Research on Prevention and Treatment, 2016, 43(12): 1018-1022. DOI: 10.3971/j.issn.1000-8578.2016.12.002

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

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  • Corresponding author:

    ZHAO Ronglan, E-mail: zhaorognlan76@sina.com

  • Received Date: February 01, 2016
  • Revised Date: June 12, 2016
  • Available Online: February 04, 2024
  • 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.

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