REGULATION OF BREAST CANCER CELL PROGRESSION: THE ROLE OF GLUTATHIONE/GLUTAREDOXIN SYSTEM

Issue: 
8
Year: 
2016

E.V. Shakhristova
Ph.D. (Med.), Associate Professor, Department of Biochemistry and Molecular Biology with the Rate of Clinical Laboratory Diagnostics,
Siberian State Medical University (Tomsk)
E-mail: shaxristova@yandex.ru
E.A. Stepovaya
Dr.Sc. (Med.), Professor, Department of Biochemistry and Molecular Biology with the Rate of Clinical Laboratory Diagnostics,
Siberian State Medical University (Tomsk)
N.V. Ryazantseva
Dr.Sc. (Med.), Professor, Department of Biophysics,
Institute of Basic Biology and Biotechnology of Siberian Federal University (Krasnoyarsk);
Department of Biological Chemistry with courses of Medical, Pharmaceutical and Toxicological Chemistry,
Krasnoyarsk State Medical University
O.L. Nosareva
Ph.D. (Med.), Associate Professor, Department of Biochemistry and Molecular Biology with the Rate of Clinical Laboratory Diagnostics,
Siberian State Medical University (Tomsk)
R.I. Chil'chigashev
Student, Medical and Biological Faculty, Siberian State Medical University (Tomsk)
M.Yu. Egorova
Student, Medical Faculty, Siberian State Medical University (Tomsk)

Investigation of the role of redox-modulation by glutathione and glutaredoxin systems in regulatory activity of different cell proteins, including cyclins and cyclin-dependent kinase – modulators of proliferation, is a new trend. This trend is very perspective for searching molecular markers of socially significant diseases and investigating breast tumor transformation that make the biggest part of cancer incidence among women in the world and in Russia, in particular. The role of the glutathione/glutaredoxin system in molecular mechanisms of regulating MCF-7 breast cancer cell proliferation under the effect of N-ethylmaleimide – an SH group and peptide inhibitor – was evaluated. Cell culture in the presence of N-ethylmaleimide resulted in a decrease in the redox potential of the glutathione system, a rise in the glutaredoxin level and S-phase arrest induced by cyclin-dependent kinase 4. The obtained results may be further used for developing personalized approaches to diagnostics and treatment of breast tumors.
Keywords: 
Key words: proliferation
cell redox status
glutaredoxin
glutathione
breast adenocarcinoma cells
oxidative stress.