| Summary: | 碩士 === 國立中興大學 === 生物化學研究所 === 101 === Breast cancer is the fourth leading cause of death of female in Taiwan, The current treatment of patients with breast cancer target estrogen receptor (ER), progesterone receptor (PR) and human epidermal growth factor type II (HER-2) receptor type and other tumor markers for personalized medicine. However, triple negative breast cancer (TNBC) is a non-specific receptor expression and is therefore not suitable for use of hormone therapy and targeted therapy, currently there is no specific clinical treatment. Tamoxifen is one of the most widely used chemotherapeutic agents for the treatment of estrogen receptor (ER)-positive breast cancer patients. The main mechanism of tamoxifen has been demonstrated to induce apoptosis and reduce cell proliferation in tumor cells via inhibition of ER signaling. In this study, we used CSC-3436, a derivatives of 2-phenylnaphthyridin-4-ones (2-PN) to address the hypothesis that the CSC-3436 will sensitize TNBC cells to tamoxifen. The results showed that CSC-3436 reduced cell viability and cell proliferation in TNBC, MDA-MB-231, BT-20 and BT-549 cell lines. CSC-3436 enhanced the anticancer effect of tamoxifen through inducing apoptosis in TNBC cells. We also found that CSC-3436 inhibited TNBC cells metastasis, Epithelial-Mesenchymal Transition (EMT), and reduced the transforming growth factor beta receptor-II (TGFβR-II), as well as downstream p-Samd signal transduction and other effects. CSC-3436 synergized with Tamoxifen against TNBC cells through the induction of apoptosis.
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