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Sulforaphane Decrease of SERTAD1 Expression Triggers G1/S Arrest in Breast Cancer Cells

Journal of Medicinal Food 2019년 22권 5호 p.444 ~ 450
Cheng An-Chin, Shen Ching-Ju, Hung Chao-Ming, Hsu Yi-Chiang,
소속 상세정보
 ( Cheng An-Chin ) - Chang Jung Christian University College of Health Science Department of Nutrition and Health Science
 ( Shen Ching-Ju ) - Kaohsiung Medical University Kaohsiung Medical University Hospital Department of Gynecology and Obstetrics
 ( Hung Chao-Ming ) - I-Shou University E-Da Hospital Department of General Surgery
 ( Hsu Yi-Chiang ) - Chang Jung Christian University College of Health Science Department of Medical Sciences Industry

Abstract


Studies have identified the potential of chemopreventive effects of sulforaphane (SFN); however, the underlying mechanisms of its effect on breast cancer require further elucidation. This study investigated the anticancer effects of SFN that specifically induces G1/S arrest in breast ductal carcinoma (ZR-75-1) cells. The proliferation of the cancer cells after treatment with SFN was detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. DNA content and cell cycle status were analyzed through flow cytometry. Our results demonstrated the inhibition of growth in ZR-75-1 cells upon SFN exposure. In addition, SERTAD1 (SEI-1) caused the accumulation of SFN-treated G1/S-phase cells. The downregulation of SEI-1, cyclin D2, and histone deacetylase 3 suggested that in addition to the identified effects of SFN against breast cancer prevention, it may also exert antitumor activities in established breast cancer cells. In conclusion, SFN can inhibit growth of and induce cell cycle arrest in cancer cells, suggesting its potential role as an anticancer agent.

키워드

breast cancer; G1/S arrest; SERTAD1; sulforaphane

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