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

被引：19

作者：

Cheng, An-Chin ^{[1
]}

Shen, Ching-Ju ^{[3
]}

Hung, Chao-Ming ^{[4
]}

Hsu, Yi-Chiang ^{[2
]}

机构：

[1] Chang Jung Christian Univ, Dept Nutr & Hlth Sci, 1 Changda Rd, Tainan 71101, Taiwan

[2] Chang Jung Christian Univ, Coll Hlth Sci, Dept Med Sci Ind, 1 Changda Rd, Tainan 71101, Taiwan

[3] Kaohsiung Med Univ, Kaohsiung Med Univ Hosp, Dept Gynecol & Obstet, Kaohsiung, Taiwan

[4] I Shou Univ, E Da Hosp, Dept Gen Surg, Kaohsiung, Taiwan

来源：

JOURNAL OF MEDICINAL FOOD | 2019年 / 22卷 / 05期

关键词：

breast cancer; G1; S arrest; SERTAD1; sulforaphane; CYCLIN D2 EXPRESSION; PROTEIN P34(SEI-1); TRIP-BR; BRASSICA; INHIBITION; APOPTOSIS; PATHWAYS; SEI-1; PHASE;

D O I：

10.1089/jmf.2018.4195

中图分类号：

R914 [药物化学];

学科分类号：

100701 ;

摘要：

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.

引用

页码：444 / 450

页数：7

共 35 条

[1] Breast cancer risk in premenopausal women is inversely associated with consumption of broccoli, a source of isothiocyanates, but is not modified by GST genotype [J].

Ambrosone, CB ;

McCann, SE ;

Freudenheim, JL ;

Marshall, JR ;

Zhang, YS ;

Shields, PG .

JOURNAL OF NUTRITION, 2004, 134 (05) :1134-1138

[2]

Amjad Ali I, 2015, Curr Pharmacol Rep, V1, P382

[3]

Atwell Lauren L, 2015, Curr Pharmacol Rep, V1, P102

[4] Pathways governing G1/S transition and their response to DNA damage [J].

Bartek, J ;

Lukas, J .

FEBS LETTERS, 2001, 490 (03) :117-122

[5] Differential effects of sulforaphane on histone deacetylases, cell cycle arrest and apoptosis in normal prostate cells versus hyperplastic and cancerous prostate cells [J].

Clarke, John D. ;

Hsu, Anna ;

Yu, Zhen ;

Dashwood, Roderick H. ;

Ho, Emily .

MOLECULAR NUTRITION & FOOD RESEARCH, 2011, 55 (07) :999-1009

[6] Preclinical and clinical evaluation of sulforaphane for chemoprevention in the breast [J].

Cornblatt, Brian S. ;

Ye, Lingxiang ;

Dinkova-Kostova, Albena T. ;

Erb, Melanie ;

Fahey, Jed W. ;

Singh, Navin K. ;

Chen, Min-Shue A. ;

Stierer, Tracey ;

Garrett-Mayer, Elizabeth ;

Argani, Pedram ;

Davidson, Nancy E. ;

Talalay, Paul ;

Kensler, Thomas W. ;

Visvanathan, Kala .

CARCINOGENESIS, 2007, 28 (07) :1485-1490

[7]

Evron E, 2001, CANCER RES, V61, P2782

[8] Normal Proliferation and Tumorigenesis but Impaired Pancreatic Function in Mice Lacking the Cell Cycle Regulator Sei1 [J].

Fernandez-Marcos, Pablo J. ;

Pantoja, Cristina ;

Gonzalez-Rodriguez, Agueda ;

Martin, Nicholas ;

Flores, Juana M. ;

Valverde, Angela M. ;

Hara, Eiji ;

Serrano, Manuel .

PLOS ONE, 2010, 5 (01)

[9]

Fowke JH, 2003, CANCER RES, V63, P3980

[10] Comparison of genomic abnormalities between BRCAX and sporadic breast cancers studied by comparative genomic hybridization [J].

Gronwald, J ;

Jauch, A ;

Cybulski, C ;

Schoell, B ;

Böhm-Steuer, B ;

Lener, M ;

Grabowska, E ;

Górski, B ;

Jakubowska, A ;

Domagala, W ;

Chosia, M ;

Scott, RJ ;

Lubinski, J .

INTERNATIONAL JOURNAL OF CANCER, 2005, 114 (02) :230-236

← 1 2 3 4 →