Genistein inhibits MDA-MB-231 triple-negative breast cancer cell growth by inhibiting NF-κB activity via the Notch-1 pathway

International Journal of Molecular Medicine
Hong PanShui Wang

Abstract

Genistein (Gen) has been reported as a protective factor against breast cancer. However, the molecular mechanism by which Gen elicits its effects on triple-negative breast cancer cells has not been fully elucidated. In our study, the breast cancer cell line MDA-MB-231 was selected to determine the action of Gen on triple-negative breast cancer cells. MTT assay, flow cytometric analysis, siRNA transfection, western blotting and nuclear factor-κB (NF-κB) activation-nuclear translocation assay were used to address the role of NF-κB activity and the Notch-1 signaling pathway on the effects of Gen. Our study revealed that Gen elicited a dramatic effect on cell growth inhibition, in a dose-dependent and time-dependent manner. Treatment of MDA-MB-231 cells with 0, 5, 10 or 20 µM Gen induced apoptosis of 6.78, 18.98, 30.45 and 60.64%, respectively. Exposure of MDA-MB-231 cells to Gen also resulted in G2/M phase accumulation of cells corresponding to 4.93, 12.54, 18.93 and 30.95%, respectively. Furthermore, our data demonstrated for the first time that Gen inhibited the growth of MDA-MB-231 triple-negative breast cancer cells by inhibiting NF-κB activity via the Nocth-1 signaling pathway in a dose-dependent manner. We also found that Ge...Continue Reading

References

Jan 31, 1998·The Journal of Clinical Investigation·M A SovakG E Sonenshein
Apr 7, 1998·Molecular and Cellular Biology·F OswaldR M Schmid
Mar 18, 1999·The American Journal of Pathology·G E GrayS Artavanis-Tsakonas
Nov 14, 2002·Current Problems in Cancer·Harikrishna Nakshatri, Robert J Goulet
Jul 2, 2003·Leukemia·P ViatourV Bours
Nov 13, 2003·Seminars in Oncology·Shaomeng WangMarc E Lippman
Feb 3, 2006·Cancer Research·Spyros StylianouKeith Brennan
Jun 8, 2006·JAMA : the Journal of the American Medical Association·Lisa A CareyRobert C Millikan
Nov 23, 2006·Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology·Bruce G HafftyDeborah Toppmeyer
Dec 6, 2006·Cancer·Emad A RakhaIan O Ellis
Mar 3, 2007·Cancer Research·Ie-Ming Shih, Tian-Li Wang
May 18, 2007·Modern Pathology : an Official Journal of the United States and Canadian Academy of Pathology, Inc·Brendan C DicksonMichael Reedijk
Jul 26, 2007·BMC Cancer·Marc TischkowitzWilliam D Foulkes
Aug 3, 2007·Clinical Cancer Research : an Official Journal of the American Association for Cancer Research·Rebecca DentSteven A Narod
Nov 9, 2007·Breast Cancer Research and Treatment·Michael ReedijkIrene L Andrulis
Jan 10, 2008·British Journal of Cancer·A H WuM C Pike
Jul 3, 2008·British Journal of Cancer·A H WuM C Yu
Aug 14, 2008·Expert Review of Anticancer Therapy·Lucio Miele
Sep 2, 2008·Toxicology in Vitro : an International Journal Published in Association with BIBRA·Zhong LiJida Xu
May 1, 2009·The American Journal of Clinical Nutrition·Sang-Ah LeeWei Zheng
Dec 10, 2009·JAMA : the Journal of the American Medical Association·Xiao Ou ShuWei Lu
Jul 9, 2010·CA: a Cancer Journal for Clinicians·Ahmedin JemalElizabeth Ward

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Citations

Nov 26, 2013·Tumour Biology : the Journal of the International Society for Oncodevelopmental Biology and Medicine·Zhanzhao FuTao Gu
Dec 26, 2015·Molecules : a Journal of Synthetic Chemistry and Natural Product Chemistry·Alina UifăleanCristina Adela Iuga
Mar 10, 2016·Chemico-biological Interactions·Nour H AboalhaijaMutasem O Taha
Aug 25, 2016·Nutrients·Yue ZhouHua-Bin Li
Oct 5, 2017·International Journal of Cancer. Journal International Du Cancer·Lokesh Dalasanur NagaprashanthaSharad S Singhal
Jun 8, 2018·Phytotherapy Research : PTR·Harini Anandhi SenthilkumarEdward J Kennelly
Apr 1, 2016·British Journal of Cancer·Carlos Martínez-PérezSimon P Langdon
Aug 12, 2014·Biochemical Society Transactions·Carlos Martinez-PerezSimon P Langdon
Sep 13, 2019·Critical Reviews in Food Science and Nutrition·Haroon KhanHui Cao
Sep 22, 2019·International Journal of Molecular Sciences·Itika AroraTrygve O Tollefsbol
Dec 14, 2018·Experimental and Therapeutic Medicine·Xiaoping RuiYao Yao
Jan 1, 2014·SAGE Open Medicine·Abed AgbaryaJamal Mahajna
Jul 8, 2017·Current Medicinal Chemistry·Manee Patanapongpibul, Qiao-Hong Chen
Jan 2, 2019·Cancers·Mariam AbotalebDietrich Büsselberg
Jul 6, 2019·Daru : Journal of Faculty of Pharmacy, Tehran University of Medical Sciences·Nazanin Momeni RoudsariAmir Hossein Abdolghaffari
Apr 24, 2015·European Journal of Drug Metabolism and Pharmacokinetics·Nuggehally R Srinivas
Oct 6, 2020·Frontiers in Nutrition·Ornella I SelminDonato F Romagnolo
Jul 29, 2017·Phytotherapy Research : PTR·Marcello IritiRobert D Wojtyczka
Jan 29, 2020·Bioscience Reports·Hui ZhangZhiyi Chen
Jun 11, 2020·Cancers·Assunta SellittoFrancesca Rizzo
Jan 16, 2016·Nutrition and Cancer·Columba de la ParraSuranganie Dharmawardhane
Jan 5, 2018·Bioscience Reports·Naveen K R Chalakur-Ramireddy, Suresh B Pakala
Jan 12, 2021·Saudi Journal of Biological Sciences·Domínguez-Arispuro Dulce-MaríaCuevas-Rodríguez Edith-Oliva
Dec 16, 2020·Journal of Controlled Release : Official Journal of the Controlled Release Society·Nilesh MalaviaSanyog Jain
Jul 22, 2019·Cancer Letters·B Madhu KrishnaSharad S Singhal
Apr 28, 2020·Phytomedicine : International Journal of Phytotherapy and Phytopharmacology·Rama Rao MallaVenkata Ramesh Dasari

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