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Published on: June 9, 2023
Sinensetin suppresses breast cancer cell progression via Wnt/β-catenin pathway inhibition
Shengqian Zhu1, Lifei Meng2, Peng Wei1
1Department of Plastic and Reconstructive Surgery, The First Affiliated Hospital of Ningbo University, Ningbo, China.
Background:
Although there are many treatments for breast cancer, such as surgery, radiotherapy, chemotherapy, estrogen receptor antagonists, immune checkpoint inhibitors and so on. However, safer and more effective therapeutic drugs for breast cancer are needed. Sinensetin, a safer therapeutic drugs, come from citrus species and medicinal plants used in traditional medicine, while its role and underlying mechanism in breast cancer remain unclear. Our study aimed to investigate the role and mechanism of sinensetin in breast cancer.
Methods:
Cell Counting Kit-8 (CCK-8) was used to determine the safe concentration of sinensetin in MCF-10A, MCF7 and MDA-MB-231 cells; 120 μM sinensetin was used in subsequent experiments. Real time polymerase chain reaction (RT-PCR), Western blotting, Terminal Deoxynucleotidyl Transferase mediated dUTP Nick-End Labeling (TUNEL) apoptosis assay, Transwell invasion assay and Clone formation assay were used in this study to determine cell viability, mRNA expression, protein levels, apoptosis, proliferation, invasion and so on.
Results:
Herein, our results showed that 120 μM sinensetin suppressed the cell viability and promoted apoptosis of MCF7 and MDA-MB-231 cells. Treatment with 120 µM sinensetin for 24 h showed no significant toxicity to normal mammary cells; 120 μM sinensetin decreased cell proliferation, invasion, and epithelial-mesenchymal transition (EMT), and downregulated β-catenin, lymphatic enhancing factor 1 (LEF1), T-cell factor (TCF) 1/TCF7, and TCF3/TCF7L1 expression in MCF7 and MDA-MB-231 cells. The Wnt agonist SKL2001 reversed the inhibitory effect of sinensetin on cell survival, metastasis, and EMT. Sinensetin-induced downregulation of β-catenin, LEF1, and TCF1/TCF7 expression were upregulated by SKL2001 in MCF7 and MDA-MB-231 cells.
Conclusions:
In summary, sinensetin suppressed the metastasis of breast cancer cell via inhibition of Wnt/β-catenin pathway and there were no adverse effects on normal breast cells. Our study confirmed the role of sinensetin in breast cancer cells and provided a better understanding of the underlying mechanism.
Insights
Sinensetin, a natural compound, effectively suppresses breast cancer metastasis by inhibiting the Wnt/β-catenin pathway. This study demonstrates sinensetin
Area of Science:
- Oncology
- Pharmacology
- Molecular Biology
Background:
- Existing breast cancer treatments have limitations, necessitating novel therapeutic agents.
- Sinensetin, derived from citrus and medicinal plants, shows potential but its mechanism in breast cancer is unknown.
Purpose of the Study:
- To investigate the role and underlying mechanism of sinensetin in breast cancer.
- To evaluate sinensetin's efficacy and safety as a breast cancer therapeutic.
Main Methods:
- Cell Counting Kit-8 (CCK-8) assay for safe concentration determination.
- RT-PCR, Western blotting, TUNEL assay, Transwell invasion, and clone formation assays were employed.
- Wnt agonist SKL2001 was used to validate the Wnt/β-catenin pathway involvement.
Main Results:
- Sinensetin (120 μM) suppressed viability and promoted apoptosis in MCF7 and MDA-MB-231 breast cancer cells.
- Sinensetin reduced proliferation, invasion, and epithelial-mesenchymal transition (EMT), downregulating Wnt/β-catenin pathway components.
- No significant toxicity was observed in normal breast cells (MCF-10A).
Conclusions:
- Sinensetin inhibits breast cancer metastasis by targeting the Wnt/β-catenin pathway.
- Sinensetin represents a potentially safe and effective therapeutic agent for breast cancer.
- This study elucidates sinensetin's mechanism, offering a new understanding for breast cancer treatment.
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