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Isolation and Functional Assessment of Human Breast Cancer Stem Cells from Cell and Tissue Samples
Published on: October 2, 2020
Astaxanthin Reduces Stemness Markers in BT20 and T47D Breast Cancer Stem Cells by Inhibiting Expression of Pontin and
Yong Tae Ahn1, Min Sung Kim2, Youn Sook Kim3
1Research Institute for Longevity and Well-Being, Pusan National University, Busan 46241, Korea.
Abstract:
Astaxanthin (AST) is a product made from marine organisms that has been used as an anti-cancer supplement. It reduces pontin expression and induces apoptosis in SKBR3, a breast cancer cell line. Using Western blotting and qRT-PCR analyses, this study revealed that in the T47D and BT20 breast cancer cell lines, AST inhibits expression of pontin and mutp53, as well as the Oct4 and Nanog cancer stem cell (CSC) stemness genes. In addition, we explored the mechanism by which AST eradicates breast cancer cells using pontin siRNAs. Pontin knockdown by pontin siRNA reduced proliferation, Oct4 and Nanog expression, colony and spheroid formation, and migration and invasion abilities in breast cancer cells. In addition, reductions in Oct4, Nanog, and mutp53 expression following rottlerin treatment confirmed the role of pontin in these cells. Therefore, pontin may play a central role in the regulation of CSC properties and in cell proliferation following AST treatment. Taken together, these findings demonstrate that AST can repress CSC stemness genes in breast cancer cells, which implies that AST therapy could be used to improve the efficacy of other anti-cancer therapies against breast cancer cells.
Insights
Astaxanthin (AST) inhibits cancer stemness genes in breast cancer cells by reducing pontin expression. This suggests AST therapy can enhance other anti-cancer treatments.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Astaxanthin (AST), a marine-derived compound, exhibits anti-cancer properties.
- Pontin, mutp53, Oct4, and Nanog are implicated in cancer cell proliferation and stemness.
Purpose of the Study:
- To investigate the effect of AST on pontin expression and cancer stem cell (CSC) properties in breast cancer.
- To elucidate the mechanism by which AST impacts breast cancer cell behavior.
Main Methods:
- Western blotting and qRT-PCR to analyze gene expression.
- ব্যবহার of pontin siRNAs to knockdown pontin expression.
- Cell proliferation, colony formation, spheroid formation, migration, and invasion assays were performed.
Main Results:
- AST inhibited pontin, mutp53, Oct4, and Nanog expression in T47D and BT20 breast cancer cell lines.
- Pontin knockdown reduced breast cancer cell proliferation, stemness gene expression, colony/spheroid formation, and migration/invasion.
- Rottlerin treatment confirmed pontin's role in regulating Oct4, Nanog, and mutp53 expression.
Conclusions:
- Pontin plays a key role in regulating CSC properties and proliferation in breast cancer cells treated with AST.
- AST represses CSC stemness genes, indicating its potential to improve the efficacy of other anti-cancer therapies.
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