Affiliations: MOE Key Laboratory of Laser Life Science and Institute
of Laser Life Science, South China Normal University, Guangzhou, China | Department of Anesthesiology, The First Affiliated
Hospital of Jinan University, Guangzhou, China | Key Laboratory of Optoelectronic Science and
Technology for Medicine, Fujian Normal University, Ministry of Education,
Fuzhou, China
Note: [] Corresponding author: Prof. Tong-sheng Chen, Ph.D., Institute of
Laser Life Science, South China Normal University, Guangzhou 510631, China.
Tel.: +86 20 85211421 8606; 86 13434292240; Fax: +86 20 85216052; E-mail:
[email protected]
Abstract: Taxol (Paclitaxel) is an important natural product for the treatment
of solid tumors such as ovarian, breast, non-small-cell lung tumors, and some
head and neck carcinomas. Different concentrations of taxol trigger distinct
effects on cell death forms. In present study, cell counting kit (CCK-8) assay,
confocal fluorescence microscopy imaging, flow cytometry (FCM) and western
blotting (WB) analysis were used to analyze the characteristics of cell death
induced by low (35 nM) and high (70 μM) concentration of
taxol respectively in human lung adenocarcinoma (ASTC-a-1) cells. Our results
showed that low concentration of taxol induced cell death dominantly in
apoptotic fashion associated with nuclear fragmentation, protein synthesis,
phosphatidylserine (PS) externalization, G2/M cell cycle arrest, Bax
translocation into mitochondria and caspase-3 activation, whereas high
concentration of this drug induced significant cytoplasm vacuolization,
mitochondria swelling and paraptosis-like cell death form without protein
synthesis that is necessary for paraptosis. Although the mechanism of high
concentration of taxol-induced paraptosis-like cell death has not been clear,
this finding might have a potential implication for cancer therapy, especially
for apoptosis-resistant cancer.
Keywords: Taxol, caspase-3, apoptosis, paraptosis, protein synthesis
