Open Access

Potential therapeutic mechanism of genistein in breast cancer involves inhibition of cell cycle regulation

  • Authors:
    • Ling Zhang
    • Bo Yang
    • Ke Zhou
    • Hua Li
    • Dong Li
    • Hui Gao
    • Tao  Zhang
    • Dong Wei
    • Zhihui Li
    • Yong Diao
  • View Affiliations

  • Published online on: November 10, 2014     https://doi.org/10.3892/mmr.2014.2907
  • Pages: 1820-1826
  • Copyright: © Zhang et al. This is an open access article distributed under the terms of Creative Commons Attribution License [CC BY_NC 3.0].

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

Genistein can prevent tumorigenesis and reduce the incidence of diseases that are dependent upon estrogen. Previous research, however, has shown that genistein can also increase the risk of breast cancer. Thus, the aim of the present study was to investigate the mechanism underlying the effect of genistein in breast cancer and to determine whether genistein produces a therapeutic effect or promotes the development of breast cancer. Gene microarray data obtained from three samples treated with alcohol (control group), three samples treated with 3 µmol/l genistein and three samples treated with 10 µmol/l genistein for 48 h, were downloaded from the Gene Expression Omnibus database. Analysis of the differentially expressed genes (DEGs) and functional enrichment in the two genistein groups was performed. The interaction networks of the DEGs were constructed and the overlapping network was extracted. Finally, the functions and pathways of the DEGs in the overlapping network were enriched. In total, 224 DEGs coexisted in the two genistein groups, and the most significant function of these was the cell cycle. The number and the fold change of expression values of the DEGs in the 10 µmol/l genistein group were significantly higher compared with that of the 3 µmol/l genistein group. The most significant function and pathway of the DEGs in the overlapping network was the cell cycle involving several genes, including GLIPR1, CDC20, BUB1, MCM2 and CCNB1. Thus, genistein stimulation resulted in gene expression changes in breast cancer cell lines and discrepancies increased with higher doses of genistein. The DEGs were most significantly associated with cell cycle regulation.
View Figures
View References

Related Articles

Journal Cover

March-2015
Volume 11 Issue 3

Print ISSN: 1791-2997
Online ISSN:1791-3004

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Zhang L, Yang B, Zhou K, Li H, Li D, Gao H, Zhang T, Wei D, Li Z, Diao Y, Diao Y, et al: Potential therapeutic mechanism of genistein in breast cancer involves inhibition of cell cycle regulation. Mol Med Rep 11: 1820-1826, 2015
APA
Zhang, L., Yang, B., Zhou, K., Li, H., Li, D., Gao, H. ... Diao, Y. (2015). Potential therapeutic mechanism of genistein in breast cancer involves inhibition of cell cycle regulation. Molecular Medicine Reports, 11, 1820-1826. https://doi.org/10.3892/mmr.2014.2907
MLA
Zhang, L., Yang, B., Zhou, K., Li, H., Li, D., Gao, H., Zhang, T., Wei, D., Li, Z., Diao, Y."Potential therapeutic mechanism of genistein in breast cancer involves inhibition of cell cycle regulation". Molecular Medicine Reports 11.3 (2015): 1820-1826.
Chicago
Zhang, L., Yang, B., Zhou, K., Li, H., Li, D., Gao, H., Zhang, T., Wei, D., Li, Z., Diao, Y."Potential therapeutic mechanism of genistein in breast cancer involves inhibition of cell cycle regulation". Molecular Medicine Reports 11, no. 3 (2015): 1820-1826. https://doi.org/10.3892/mmr.2014.2907