Objective: To study the relationship between the expression of TRβ1 and the molecular typing and clinicopathological features of breast cancer.
Methods: The expression of TRβ1, ER, PR and HER-2 proteins in 208 cases of invasive breast cancer, 52 intraductal carcinoma and 22 normal breast tissue was detected by immunohistochemistry in order to analyze the relationship between the expression of TRβ1 protein and clinicopathological parameters of breast cancer. Western blot was performed to detect the effect of TRβ1 silencing on the expression of Notch signaling pathway proteins and Epithelial-mesenchymal transition (EMT)-related proteins in MCF-7 cells.
Results: In the 208 cases of invasive breast cancer tissues, over expression of TRβ1 protein was found in 88 cases while low expression in 120 cases, and the immunohistochemical score was (3.9±3.1). TRβ1 protein was found over expressed in all the 52 cases of intraductal carcinoma and 22 cases of normal breast tissue, with the immunohistochemical score of (9.7±2.1) and 12.0, respectively, and there was no significant difference between the two groups (P>0.05) while both of them were significantly lower than the invasive breast cancer group (P<0.05). The expression of TRβ1 protein in the invasive breast cancer tissues was significantly correlated with lymph node metastasis (P=0.041), molecular typing (P=0.037) and histological grade (P<0.001) while it was negatively correlated with HER-2 expression (r=0.926; P<0.001) and irrelevant with age (P=1.024), ER expression (P=0.834), PR expression (P=0.351) or TNM staging (P=1.032). Compared to normal MCF-7 cells, the expression of Notch1, Dell 1, Jagged-1 and vimentin proteins increased by 1.44 times, 1.53 times, 1.50 times and 1.45 times respectively in the TRβ1 expression silenced MCF-7 cell.
Conclusions: The expression of TRβ1 protein in breast cancer tissues decreased with the increase of HER-2 expression and histological grade. The depletion of TRβ1 protein may activate the Notch signaling pathway and enhance the EMT ability of breast cancer cells thus promoting the cancer cell migration.
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