Qualitative and Quantitative Analysis of ROS-Mediated Oridonin-Induced Oesophageal Cancer KYSE-150 Cell Apoptosis by Atomic Force Microscopy.
High levels of intracellular reactive oxygen species (ROS) in cells is recognized as one of the major causes of cancer cell apoptosis and has been developed into a promising therapeutic strategy for cancer therapy. However, whether apoptosis associated biophysical properties of cancer cells are related to intracellular ROS functions is still unclear. Here, for the first time, we determined the changes of biophysical properties associated with the ROS-mediated oesophageal cancer KYSE-150 cell apoptosis using high resolution atomic force microscopy (AFM). Oridonin was proved to induce ROS-mediated KYSE-150 cell apoptosis in a dose dependent manner, which could be reversed by N-acetylcysteine (NAC) pretreatment. Based on AFM imaging, the morphological damage and ultrastructural changes of KYSE-150 cells were found to be closely associated with ROS-mediated oridonin-induced KYSE-150 cell apoptosis. The changes of cell stiffness determined by AFM force measurement also demonstrated ROS-dependent changes in oridonin induced KYSE-150 cell apoptosis. Our findings not only provided new insights into the anticancer effects of oridonin, but also highlighted the use of AFM as a qualitative and quantitative nanotool to detect ROS-mediated cancer cell apoptosis based on cell biophysical properties, providing novel information of the roles of ROS in cancer cell apoptosis at nanoscale.
State Key Laboratory of Quality Research in Chinese Medicines, Macau University of Science and Technology, Macau, China.
Jiang
J
Pi
Department of Chemistry, Jinan University, GuangZhou, China.
Huaihong
H
Cai
State Key Laboratory of Quality Research in Chinese Medicines, Macau University of Science and Technology, Macau, China.
Hua
H
Jin
State Key Laboratory of Quality Research in Chinese Medicines, Macau University of Science and Technology, Macau, China.
Fen
F
Yang
State Key Laboratory of Quality Research in Chinese Medicines, Macau University of Science and Technology, Macau, China.
Jinhuan
J
Jiang
State Key Laboratory of Quality Research in Chinese Medicines, Macau University of Science and Technology, Macau, China.
Anguo
A
Wu
Department of Chemistry, Jinan University, GuangZhou, China.
Haiyan
H
Zhu
Department of Chemistry, Jinan University, GuangZhou, China; Department of Pharmacology, Hunan University of Medicine, HuaiHua, China.
Jianxin
J
Liu
State Key Laboratory of Quality Research in Chinese Medicines, Macau University of Science and Technology, Macau, China.
Xiaohui
X
Su
State Key Laboratory of Quality Research in Chinese Medicines, Macau University of Science and Technology, Macau, China.
Peihui
P
Yang
State Key Laboratory of Quality Research in Chinese Medicines, Macau University of Science and Technology, Macau, China.
Jiye
J
Cai
D000111:Acetylcysteine / Q000494:pharmacology; D000972:Antineoplastic Agents, Phytogenic / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects*; D045744:Cell Line, Tumor; D045786:Diterpenes, Kaurane / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D004847:Epithelial Cells / Q000187:drug effects* / Q000378:metabolism / Q000648:ultrastructure; D004947:Esophagus / Q000187:drug effects / Q000378:metabolism / Q000648:ultrastructure; D016166:Free Radical Scavengers / Q000494:pharmacology; D006801:Humans; D053078:Membrane Potential, Mitochondrial / Q000187:drug effects; D018625:Microscopy, Atomic Force; D008928:Mitochondria / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D018384:Oxidative Stress; D017382:Reactive Oxygen Species / Q000819:agonists / Q000037:antagonists & inhibitors / Q000378:metabolism*
D000972:Antineoplastic Agents, Phytogenic; D045786:Diterpenes, Kaurane; D016166:Free Radical Scavengers; D017382:Reactive Oxygen Species; C011959:oridonin; D000111:Acetylcysteine