Potential therapeutic mechanism of genistein in breast cancer involves inhibition of cell cycle regulation.
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.
Department of Radiotherapy, Chengdu Military General Hospital, Chengdu, Sichuan 610083, P.R. China.
Ling
L
Zhang
Department of Oncology, Chengdu Military General Hospital, Chengdu, Sichuan 610083, P.R. China.
Bo
B
Yang
PET‑CT Center, Chengdu Military General Hospital, Chengdu, Sichuan 610083, P.R. China.
Ke
K
Zhou
Department of Oncology, Chengdu Military General Hospital, Chengdu, Sichuan 610083, P.R. China.
Hua
H
Li
Department of Oncology, Chengdu Military General Hospital, Chengdu, Sichuan 610083, P.R. China.
Dong
D
Li
Department of Oncology, Chengdu Military General Hospital, Chengdu, Sichuan 610083, P.R. China.
Hui
H
Gao
Department of Oncology, Chengdu Military General Hospital, Chengdu, Sichuan 610083, P.R. China.
Tao
T
Zhang
Department of Oncology, Chengdu Military General Hospital, Chengdu, Sichuan 610083, P.R. China.
Dong
D
Wei
Department of Radiotherapy, Chengdu Military General Hospital, Chengdu, Sichuan 610083, P.R. China.
Zhihui
Z
Li
Department of Radiotherapy, Chengdu Military General Hospital, Chengdu, Sichuan 610083, P.R. China.
Yong
Y
Diao
D016588:Anticarcinogenic Agents / Q000494:pharmacology*; D001943:Breast Neoplasms / Q000188:drug therapy / Q000235:genetics* / Q000378:metabolism*; D002453:Cell Cycle / Q000187:drug effects* / Q000235:genetics; D045744:Cell Line, Tumor; D016000:Cluster Analysis; D019295:Computational Biology; D005260:Female; D020869:Gene Expression Profiling; D015972:Gene Expression Regulation, Neoplastic / Q000187:drug effects; D053263:Gene Regulatory Networks; D019833:Genistein / Q000494:pharmacology*; D006801:Humans; D048789:Phytoestrogens / Q000494:pharmacology*; D047428:Protein Kinase Inhibitors / Q000494:pharmacology*; D015398:Signal Transduction
D016588:Anticarcinogenic Agents; D048789:Phytoestrogens; D047428:Protein Kinase Inhibitors; D019833:Genistein