AI Article Synopsis
- Breast cancer is the most commonly diagnosed cancer globally, often complicated by the presence of breast cancer stem cells (BCSCs), which hinder treatment success.
- Litchi seeds exhibit promising anti-cancer properties, and this study explores how total flavonoids from litchi seeds (TFLS) impact BCSCs both in laboratory settings and in mouse models.
- Findings reveal that TFLS significantly reduces the viability and tumor-initiating potential of BCSCs by targeting specific stem cell markers and inhibiting the Notch3 signaling pathway, suggesting a potential therapeutic role for litchi seed extracts in breast cancer treatment.
Article Abstract
Ethnopharmacological Relevance: Breast cancer has been the most commonly-diagnosed cancer worldwide, and the treatment and prognosis of which are often limited by breast cancer stem cells (BCSCs). Litchi seeds have shown good anti-cancer activity in various cancers including prostate cancer, lung cancer and breast cancer. However, the activity and underlying mechanism of Litchi seeds against BCSCs remain unknown.
Aim Of The Study: To investigate the activity and mechanism of total flavonoids of litchi seed (TFLS) against BCSCs in vitro and in vivo.
Materials And Methods: Two orthotopic xenograft mouse models were established using HCC1806 cells pretreated or untreated with TFLS to determine whether TFLS could target BCSCs in vivo. Mammosphere formation and flow cytometry assays were employed to evaluate the effect of TFLS on BCSCs in vitro. The underlying mechanism was investigated using RT-qPCR, Western blot, immunohistochemistry and immunofluorescence experiments.
Results: TFLS could significantly inhibit the viability of HCC1806, MCF-7 and HCC1937 cells in vitro and suppress the growth of HCC1806 cells in vivo. TFLS attenuated stem cell-like properties of breast cancer through reducing the percentage of CD44CD24 cells, inhibiting the mammospheres formation and down-regulating the mRNA and protein levels of cancer stem cells related markers (Oct4, Nanog, Sox2) in MCF-7 and HCC1806 cells. Meanwhile, TFLS suppressed the tumor-initiating ability of BCSCs via reducing the percentage of CD44CD24 cells in tumor and lowering tumor incidence rate in orthotopic xenograft mice. In addition, TFLS treatments restricted the expression and nuclear translocation of Notch3, subsequently down-regulated Hes1 and Runx2 expressions.
Conclusions: TFLS could suppress the growth of breast cancer and eliminate breast cancer stem cells by inhibiting the Notch3 signaling pathway.
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| http://dx.doi.org/10.1016/j.jep.2023.116133 | DOI Listing |
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