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Kanakugiol, a Compound Isolated from Lindera erythrocarpa, Promotes Cell Death by Inducing Mitotic Catastrophe after Cell Cycle Arrest

Journal of Microbiology and Biotechnology 2020년 30권 2호 p.279 ~ 286
 ( Lee Jin-Tak ) - Konkuk University Department of Bioscience and Biotechnology

 ( Chun Hyun-Woo ) - Konkuk University Department of Bioscience and Biotechnology
 ( Pham Thu-Huyen ) - Konkuk University Department of Bioscience and Biotechnology
 ( Yoon Jae-Hwan ) - Konkuk University Department of Bioscience and Biotechnology
 ( Lee Ji-Yon ) - Konkuk University Department of Bioscience and Biotechnology
 ( Choi Myoung-Kwon ) - Konkuk University Department of Bioscience and Biotechnology
류형원 ( Ryu Hyung-Won ) - Korea Research Institute of Bioscience and Biotechnology Natural Medicine Research Center
오세량 ( Oh Sei-Ryang ) - Korea Research Institute of Bioscience and Biotechnology Natural Medicine Research Center
오재욱 ( Oh Jae-Wook ) - Konkuk University Department of Stem Cell and Regenerative Biotechnology
윤도영 ( Yoon Do-Young ) - Konkuk University Department of Bioscience and Biotechnology

Abstract


A novel compound named ‘kanakugiol’ was recently isolated from Lindera erythrocarpa and showed free radical-scavenging and antifungal activities. However, the details of the anticancer effect of kanakugiol on breast cancer cells remain unclear. We investigated the effect of kanakugiol on the growth of MCF-7 human breast cancer cells. Kanakugiol affected cell cycle progression, and decreased cell viability in MCF-7 cells in a dose-dependent manner. It also enhanced PARP cleavage (50 kDa), whereas DNA laddering was not induced. FACS analysis with annexin V-FITC/PI staining showed necrosis induction in kanakugiol-treated cells. Caspase-9 cleavage was also induced. Expression of death receptors was not altered. However, Bcl-2 expression was suppressed, and mitochondrial membrane potential collapsed, indicating limited apoptosis induction by kanakugiol. Immunofluorescence analysis using α- tubulin staining revealed mitotic exit without cytokinesis (4N cells with two nuclei) due to kanakugiol treatment, suggesting that mitotic catastrophe may have been induced via microtubule destabilization. Furthermore, cell cycle analysis results also indicated mitotic catastrophe after cell cycle arrest in MCF-7 cells due to kanakugiol treatment. These findings suggest that kanakugiol inhibits cell proliferation and promotes cell death by inducing mitotic catastrophe after cell cycle arrest. Thus, kanakugiol shows potential for use as a drug in the treatment of human breast cancer.

키워드

Kanakugiol; breast cancer; necrosis; mitotic catastrophe; cell cycle arrest
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