we have previously reported that taxol, a potent anticancer agent, induces caspase-independent cell death and
cytoplasmic vacuolization in human lung adenocarcinoma (ASTC-a-1) cells. However, the mechanisms of taxol-induced
cytoplasmic vacuolization are poorly understood. Reactive oxygen species (ROS) has been reported to be involved in the
taxol-induced cell death. Here, we employed confocal fluorescence microscopy imaging to explore the role of ROS in
taxol-induced cytoplasmic vacuolization. We found that ROS inhibition by addition of N-acetycysteine (NAC), a total
ROS scavenger, did not suppress these vacuolization but instead increased vacuolization. Take together, our results
showed that ROS is not a promotor of the taxol-induced cytoplasmic vacuolization.
Artesunate (ART), a semi-synthetic derivative of the sesquiterpene artemisinin extracted from the Chinese herb
Artemisia annua, exerts a broad spectrum of clinical activity against human cancers. Artemisinin-derivative combination
chemotherapy is recommended by WHO since it acts rapidly and is well tolerated and particularly effective. In present
investigation, we used CKK-8 assay to assess the inhibitory effects of ART on human lung adenocarcinoma (ASTC-a-1)
cells. Apoptotic activity of ART in ASTC-a-1 cells was detected by means of nuclear staining with Hoechst33258. In
order to monitor the activity of caspase-3 during ART-induced
ASTC-a-1 cells apoptosis, the dynamical emission
spectra of SCAT3, a FRET plasmid based on GFPs, were performed inside living cell expressed stably with SCAT3 after
ART treatment. The results showed that (1) ART could inhibit
ASTC-a-1 cells proliferation in a dose-dependent manner;
(2) chromatin condensation was observed after ART treatment for 48 h; (3) the SCAT3 inside living cells were cleaved
after ART treatment for 48 h, implying that caspase-3 was involved in the ART-induced apoptosis.
Dihydroartemisinin (DHA), a semi-synthetic derivative of artemisinin, isolated from the traditional Chinese herb
Artemisia annua, has been shown to possess promising anticancer activities and induce cancer cell death through
apoptotic pathways. However, the molecular mechanisms are not well understood. This study was investigated in human
lung adenocarconoma ASTC-a-1 cell line and aimed to determine whether the apoptotic process was mediated by Bax
activation and translocation during DHA-induced apoptosis. In this study, DHA induced a time-dependent apoptotic cell
death, which was assayed by Cell Counting Kit (CCK-8) and Hoechst 33258 staining. Detection of Bax aggregation and
translocation to mitochondria was observed in living cells which were co-transfected with GFP-Bax and Dsred-mito
plasmid using confocal fluorescence microscope technique. Overall, these results demonstrated that Bax activation and
translocation to mitochondria occurred during DHA-induced apoptosis.
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