• Users Online: 169
  • Home
  • Print this page
  • Email this page
Home About us Editorial board Ahead of print Browse Articles Search Archives Submit article Instructions Subscribe Contacts Login 
ORIGINAL ARTICLE
Year : 2018  |  Volume : 9  |  Issue : 1  |  Page : 12

Effect of genistein on apoptosis and proliferation of hepatocellular Carcinoma Hepa1-6 Cell Line


1 Research Center for Noncommunicable Diseases, Jahrom University of Medical Sciences, Jahrom, Iran
2 Department of Anatomical Sciences and Molecular Biology, Medical School, Isfahan University of Medical Sciences, Isfahan, Isfahan Province, Iran
3 Department of Student Research Committee, Jahrom University of Medical Sciences, Jahrom, Iran

Correspondence Address:
Fraidoon Kavoosi
Research Center for Noncommunicable Diseases, Medicine School, Jahrom University of Medical Sciences, Motahari Avenue, Jahrom
Iran
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijpvm.IJPVM_249_16

Rights and Permissions

Background: One of the main causes of mortality is hepatocellular carcinoma (HCC) which accounts for the third leading cause of deaths and one in forty deaths worldwide. The flavonoids, natural antioxidant compounds, account for a major group of polyphenolic compounds. One of the major isoflavones in soybean is genistein (GE) which can inhibit proliferation and induce apoptosis. Isoflavones, major type of phenolic materials, derived from dietary plants and medicinal herbs play a significant role in cancer prevention and treatment. Correlation between dietary habits and cancer risk including breast, prostate, and colon cancer has been reported. Various bioactivities of these compounds such as anticarcinogenic and antioxidant are responsible for their chemopreventive activities by which induce migration, proliferation, cell cycle arrest, and apoptosis. GE, one of the major isoflavones, is considered as a potent chemopreventive agent against cancer. The aim of this study was to investigate the inhibitory and apoptotic effects of GE on HCC Hepa1-6 cell line. Methods: Cell viability assay and cell cycle analysis with flow cytometry were used to evaluate proliferative and apoptotic effect GE. Results: GE inhibited the growth of Hepa1-6 cells and induced apoptosis with a concentration and time-dependent fashion. During GE treatment for 24, the half maximal inhibitory concentration (IC50) was 20 μM, and the maximum inhibition of cell growth was 52% (P < 0.01). The percentage of apoptotic cells with a concentration of 20 μM of GE after 24, 48, and 72 h was 35, 42, and 65%, respectively (P < 0.01). Conclusions: Our finding clearly indicated that GE can significantly inhibit proliferation of hepatocellular carcinoma Hepa 1-6 cell line and induce apoptosis in this cell line.


[FULL TEXT] [PDF]*
Print this article     Email this article
 Next article
 Previous article
 Table of Contents

 Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
 Citation Manager
 Access Statistics
 Reader Comments
 Email Alert *
 Add to My List *
 * Requires registration (Free)
 

 Article Access Statistics
    Viewed1097    
    Printed33    
    Emailed0    
    PDF Downloaded119    
    Comments [Add]    
    Cited by others 2    

Recommend this journal