Abstract
ObjectiveThe aim of this study is to investigate the anti-cancer activity and sensibilization of baicalin (BA) against breast cancer (BC) cells.MethodsThe anti-proliferation of BA in BC cell lines was evaluated by MTT and colony formation assays. Apoptotic induction of BA was measured by flow cytometry. Wound-healing and transwell assays were exploited to assess migrated and invasive inhibition of BA. Western-blot and immunofluorescence were used to study mechanisms of anti-migration and sensibilization of BA. Anti-tumor and anti-metastasis effects of BA were evaluated in subcutaneous and pulmonary metastasis mouse model of BC cells.ResultsBA significantly suppressed proliferation and induced apoptosis of BC cells in a concentration- and time-dependent manner. Additionally, BA induced cell apoptosis via the mitochondria-mediated pathway, as evidenced by cellular induction of reactive oxygen species and upregulated expression of the Bax/Bcl-2 ratio. The overall expression and nuclear translocation of NF-κB signaling pathway in BC cells were dramatically inhibited by treatment with BA. BA significantly suppressed abilities of migration and invasion in BC cells. Notably, BA sensitized BC cells to docetaxel (DXL) by suppressing the expression of survivin/Bcl-2. BA also retarded tumor growth and triggered apoptosis of tumor cells in a tumor mouse model of 4T1 cells. Furthermore, pulmonary metastasis of BC cells was distinctly suppressed by BA in a tumor mouse model of 4T1 cells.ConclusionBA effectively triggered apoptosis, inhibited metastasis, and enhanced chemosensitivity of BC, implying that BA might serve as a promising agent for the treatment of BC.
Highlights
Breast cancer (BC) is the second leading cause of cancer-related mortality among women (DeSantis et al, 2019), accounting for 208,8849 new cases and 626,679 deaths worldwide in 2018 (Ferlay et al, 2019)
The overall expression and nuclear translocation of Nuclear factor kappa B (NF-kB) signaling pathway in BC cells were dramatically inhibited by treatment with BA
BA effectively triggered apoptosis, inhibited metastasis, and enhanced chemosensitivity of BC, implying that BA might serve as a promising agent for the treatment of BC
Summary
Breast cancer (BC) is the second leading cause of cancer-related mortality among women (DeSantis et al, 2019), accounting for 208,8849 new cases and 626,679 deaths worldwide in 2018 (Ferlay et al, 2019). It is estimated that there will be 268,600 new cases of invasive BC and 41,760 deaths among American women in 2019 (Siegel et al, 2019). BC, especially triple-negative BC, which is defined by no or low expression of estrogen receptor, progesterone receptor, and human epidermal growth factor receptor 2, usually metastasizes from primary tumors to distant sites, such as the brain, lung, liver, and bone, thereby resulting in a poor prognosis and high mortality (Cheung and Ewald, 2014; Couch et al, 2015; Boire et al, 2020). Multi-drug resistance, which is referred to as low chemosensitivity, is regarded as a notable obstacle to the treatment of BC (De Angelis et al, 2019). Novel agents with improved therapeutic effects against BC are urgently needed
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