JMB-HEADER RAS-JOURNALS EIMB Pleiades Publishing

RUS

             

ENG

YearIMPACT-FACTOR
2021  1,540
2020  1,374
2019  1,023
2018  0,932
2017  0,977
2016  0,799
2015  0,662
2014  0,740
2013  0,739
2012  0,637
2011  0,658
2010  0,654
2009  0,570
2008  0,849
2007  0,805
2006  0,330
2005  0,435
2004  0,623
2003  0,567
2002  0,641
2001  0,490
2000  0,477
1999  0,762
1998  0,785
1997  0,507
1996  0,518
1995  0,502
Vol 48(2014) N 3 p. 359-370; DOI 10.1134/S0026893314030133 Full Text

K. Makowska, M.C. Estañ, I. Gañán-Gómez, M.C. Boyano-Adánez, A.I. García-Pérez, P. Sancho*

Changes in Mitochondrial Function Induced by Dequalinium Precede Oxidative Stress and Apoptosis in the Human Prostate-Cancer Cell Line PC-3

Department of Biology of Systems, University of Alcalá, Alcalá de Henares (Madrid), 28871, Spain

*pilar.sancho@uah.es
Received - 2013-10-17; Accepted - 2013-12-18

Mitochondria play central roles in diverse physiological and pathological conditions associated with cell survival and death. Delocalized lipophilic cations, such as dequalinium (DQA), are accumulated in cancer cells attracted by the highly negative mitochondrial transmembrane potential of these cells. DQA showed a potent anticancer activity in cells from different malignancies. Here, we report the effect of DQA on PC-3 prostate cancer cells. Incubation with DQA at concentrations between 1.5 and 100 μM from 24 to 48 h decreases cell viability. The decrease in cell viability together with a loss of mitochondrial transmembrane potential induced an increase in reactive oxygen species production and cell death via caspase-3 dependent apoptotic pathway. DQA was shown to cause moderate to strong cell death in a time and concentration dependent manner, causing a most advantageous effect at a concentration of 10 μM applied for a long 48 h time period, which might be a consequence of the kinetics of intracellular DQA accumulation in mitochondria, but also of the mechanisms of DQA-induced cell death. This data shows DQA as a promising agent against the human prostate cancer PC-3 cell line, activating the caspase-3 dependent apoptotic pathway. This fact might be beneficial for possible future applications in cancer therapy.

mitochondria, apoptosis, dequalinium, caspase 3, ROS, prostate, PC-3



JMB-FOOTER RAS-JOURNALS