Emodin induces apoptosis of human breast cancer cells by modulating the expression of apoptosis-related genes

Oncology Letters
Cong ZuXinyu Zheng

Abstract

The aim of this study was to investigate the effects of emodin on the proliferation of human breast cancer cells Bcap-37 and ZR-75-30. Cell viability following emodin treatment was assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The effects of emodin on apoptosis were determined by flow cytometry using Annexin V-fluorescein isothiocyanate and propidium iodide staining. Quantitative polymerase chain reaction and western blot analysis were used to determine changes in the expression of apoptotic genes and protein, respectively. The effect of emodin on the invasiveness of breast cancer cells was evaluated by Matrigel invasion assay. Treatment of breast cancer cells Bcap-37 and ZR-75-30 with emodin was observed to inhibit the growth and induced apoptosis in a time- and dose-dependent manner. Emodin reduced the level of Bcl-2 and increased levels of cleaved caspase-3, PARP, p53 and Bax. These findings indicate that emodin induces growth inhibition and apoptosis in human breast cancer cells. Emodin may be a potential therapeutic agent for the treatment of breast cancer.

References

May 18, 2001·Nature·G I Evan, K H Vousden
Mar 12, 2004·Nephrology·Cheng-Chung FangYasuhiko Tomino
Sep 15, 2004·Respirology : Official Journal of the Asian Pacific Society of Respirology·Lorriana E Leard, V Courtney Broaddus
Apr 20, 2005·Oncogene·Sandra L Harris, Arnold J Levine
Apr 25, 2008·Current Protocols in Immunology·Jagan MuppidiRichard M Siegel
Nov 9, 2010·Biochimica Et Biophysica Acta·Jennefer LindsayAndrew P Gilmore
Feb 18, 2011·Expert Opinion on Pharmacotherapy·Simon SpazzapanAndrea Veronesi
Mar 19, 2011·Cell Death and Differentiation·P N Kelly, Andreas Strasser
Apr 19, 2011·BMC Complementary and Alternative Medicine·Mireille Bright-GbebryLucile L Adams-Campbell
Jun 28, 2013·Cancer Cell International·Tianyu LiuYing-Bin Liu
Oct 26, 2013·European Journal of Cancer : Official Journal for European Organization for Research and Treatment of Cancer (EORTC) [and] European Association for Cancer Research (EACR)·Tzong-Der WayChi-Tang Ho
Jun 28, 2014·Asian Pacific Journal of Cancer Prevention : APJCP·Jia LiuXiu-Kun Lin
Aug 16, 2014·Asian Pacific Journal of Cancer Prevention : APJCP·Jia-Qi SuiMing-Jie Xie
Aug 26, 2014·Pharmacological Reports : PR·Muhammad Imran AmirzadaJian Jin
Aug 27, 2014·International Journal of Surgery·Alessandro SanguinettiNicola Avenia
Sep 11, 2014·European Journal of Pharmacology·Thacker Pooja, Devarajan Karunagaran
Sep 16, 2014·International Journal of Cancer. Journal International Du Cancer·Jacques FerlayFreddie Bray

Citations

Feb 25, 2017·The American Journal of Chinese Medicine·Hsin-Shun TsengWen-Tsong Hsieh
Feb 12, 2020·Bioscience Reports·Mingdi ZhangKejin Wu
Oct 18, 2016·Oncology Reports·Jianwei ZhuQifeng Guo
May 15, 2018·Nanomaterials·Tamara KrajnovićGoran N Kaluđerović
Aug 28, 2018·3 Biotech·Mehmet Kürşat DericiAyşegül Taylan-Özkan
Mar 11, 2021·Cancer Investigation·Prasath ManogaranAnbu Singaravelu
Jul 20, 2020·Biochimica Et Biophysica Acta. Molecular Basis of Disease·Lavanya PonnusamyRavi Manoharan
Aug 11, 2018·Biomedicine & Pharmacotherapy = Biomédecine & Pharmacothérapie·Yanxin ChenJian-Da Hu

Related Concepts

Related Feeds

BCL-2 Family Proteins

BLC-2 family proteins are a group that share the same homologous BH domain. They play many different roles including pro-survival signals, mitochondria-mediated apoptosis and removal or damaged cells. They are often regulated by phosphorylation, affecting their catalytic activity. Here is the latest research on BCL-2 family proteins.

Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis