Journal
ULTRASOUND IN MEDICINE AND BIOLOGY
Volume 40, Issue 5, Pages 990-1000Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.ultrasmedbio.2013.11.022
Keywords
Chlorin e6; Sonodynamic therapy; Apoptosis; Mitochondria; Reactive oxygen species
Funding
- National Natural Science Foundation of China [81000999, 10904087]
- Research Fund for the Doctoral Program of Higher Education of China [20100202110006]
- Fundamental Research Funds for the Central Universities [GK201302022]
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It is well accepted that sonodynamic therapy (SDT) exerts cytotoxicity and anti-tumor activity in many human tumors through the induction of cell apoptosis. The aim of the work described here was to study the effect of chlorin e6 (Ce6)-mediated SDT on human chronic myelogenous leukemia K562 cells. Our results indicate that Ce6-mediated SDT can suppress the viability of K562 cells. SDT caused apoptosis as analyzed by annexin V-phycoerythrin/7-amino-actinomycin D staining as well as cleavage of caspase 3 and the polypeptide poly(ADP-ribose) polymerase. After SDT exposure, loss of mitochondrial membrane potential, translocation of Bax from cytoplasm to mitochondria and activation of caspase 9 indicated that the mitochondrial-related apoptotic pathway might be activated. This process was accompanied by rapid generation of reactive oxygen species (ROS). Scavenging of ROS significantly blocked caspase-3 expression and the killing effect of SDT on K562 cells. Stress-activated protein kinases c-jun NH2-terminal kinase (JNK) and the p38 mitogen-activated protein kinase were activated after SDT treatment. Together, these findings indicate that Ce6-mediated SDT triggers mitochondria-and caspase-dependent apoptosis; oxidative injury may play a vital role in apoptotic signaling cascades. (E-mail: wangpan@snnu.edu.cn or lshaof@snnu.edu.cn) Crown Copyright (C) 2014 Published by Elsevier Inc. on behalf of World Federation for Ultrasound in Medicine & Biology.
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