Affiliations: MOE Key Laboratory of Laser Life Science &
Institute of Laser Life Science, South China Normal University, Guangzhou
510631, China | Department of Anesthesiology, The First Affiliated
Hospital of Jinan University, Guangzhou 510632, China
Note: [] Corresponding author. Prof. Tongsheng Chen, Institute of Laser
Life Science, South China Normal University, Guangzhou 510631, China. Tel.: +86
20 85211436 8606; Fax: +86 20 85216052; E-mail: chentsh@scnu.edu.cn
Abstract: Chan-Su (CS), a traditional Chinese medicine, is one of the most
potent Chinese medicines currently used in cancer chemoprevention and
treatment. However, the molecular mechanism of CS-induced-apoptosis is still
unclear. This study investigated the molecular mechanism of CS-induced
apoptosis using fluorescence resonance energy transfer (FRET) and confocal
fluorescence microscope techniques. CS dose-dependently inhibited cell
viability cytotoxicity, which was assayed by Cell Counting Kit (CCK-8) and
Hoechst33258 staining. Bax translocation to mitochondria was observed in single
living cell transfected with GFP-Bax plasmid. The mitochondrial membrane
potential (ΔΨ_{m}) loss was also measured in
CS-treated cells. And ASTC-a-1 cell expressed stably with SCAT3 plasmid was
used to examine if caspase-3 was activated by CS. z-VAD-fmk, a broad-caspase
spectrum inhibitor, was found to significantly reduce the inhibition of CS on
the cell viability. Overall, our data demonstrated that CS induced
ASTC-a-1cells apoptosis in a dose-dependent manner, and Bax, caspase-3 and
mitochondrial stress were involved in CS-induced apoptosis. Our findings extend
the knowledge about the cellular signaling mechanisms mediating CS-induced
apoptosis.
Keywords: Chan-Su (CS), Bax translocation, apoptosis, caspase-3, fluorescence resonance energy transfer (FRET), mitochondrial membrane potential (ΔΨ[TeX:] _{m})
