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Dual target PARP1/EZH2 inhibitors inducing excessive autophagy and producing synthetic lethality for triple-negative breast cancer therapy
Triple-negative breast cancer (TNBC) accounts for 15% of all breast cancer pathological types worldwide, and it has special biological behavior and clinicopathological characteristics [1]. Because the loss of estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2) expression is negative, endocrine therapy is basically ineffective for TNBC, and targeted therapy is not sensitive, so TNBC is also known as the terminal disease of breast cancer [2,3].
Development of novel quinoline-NO donor hybrids inducing human breast cancer cells apoptosis via inhibition of topoisomerase I
Introduction Previous research has reported that quinoline and its derivatives could inhibit the activity of topoisomerase I (Topo I), which was considered as important target for the prevention of rapid proliferation of cancer cells1, 2. Several quinoline derived Topo I inhibitors, such as camptothecin and its derivatives (1, Neratinib Maleate and Bosutinib, Figure 1), have been widely used in the clinic for decades as anti-cancer drugs.
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