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

An-Chin Cheng,Chao-Ming Hung,Yi-Chiang Hsu,Ching-Ju Shen

doi:10.1089/jmf.2018.4195

An-Chin Cheng, Chao-Ming Hung + Show 2 more

Open Access

https://doi.org/10.1089/jmf.2018.4195

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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.

Highlights

Sulforaphane (SFN), a compound within the isothiocyanate group, is a biologically active phytochemical of cruciferous vegetables that has been extensively characterized for its reported anticancer, antimicrobial, and antioxidant properties.[1]
To clarify the role of SFN in the apoptosis/necrosis of breast cancer cells, the cells were treated with SFN for 4 h followed by detecting the generation of sub-G1 cells by Annexin V-FITC and propidium iodide (PI) staining
The results revealed that the messenger RNA levels of CDK2, CDK4, and CDK6 were reduced after incubation with SFN compared with that of control group (Fig. 2A)

Summary

Introduction

Sulforaphane (SFN), a compound within the isothiocyanate group, is a biologically active phytochemical of cruciferous vegetables that has been extensively characterized for its reported anticancer, antimicrobial, and antioxidant properties.[1] In cooked broccoli and broccoli sprouts, glucoraphanin, a precursor of SFN, requires metabolic conversion to active SFN by myrosinase from gastrointestinal microflora.[2] After absorption of SFN, it is metabolized into its sequential metabolites, dithiocarbamates.[3] Some researchers have illustrated several anticancer efficacies of SFN consumption, such as in vitro and in vivo activities in reducing tumor growth, increasing cancer cell apoptosis, blocking cell cycle progression, and inhibiting signaling within tumor microenvironments.[4,5,6].

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