Differential Effect of Artemisinin Against Cancer Cell Lines

Abstract

The present study aims at defining the differential cytotoxicity effect of artemisinin toward P815 (murin mastocytoma) and BSR (kidney adenocarcinoma of hamster) cell lines. Cytotoxicity was measured by the growth inhibition using MTT assay. These in vitro cytotoxicity studies were complemented by the determination of apoptotic DNA fragmentation and Annexin V- streptavidin-FITC assay. Furthermore, we examined the in vitro synergism between artemisinin and the chemotherapeutic drug, vincristin. The in vivo study was investigated using the DBA2/P815 (H2d) mouse model. While artemisinin acted on both tumor cell lines, P815 was much more sensitive to this drug than BSR cells, as revealed by the respective IC50 values (12 µM for P815 and 52 µM for BSR cells). On another hand, and interestingly, apoptosis was induced in P815 but not induced in BSR. These data, reveal an interesting differential cytotoxic effect, suggesting the existence of different molecular interactions between artemisinin and the studied cell lines. In vivo, our results clearly showed that the oral administration of artemisinin inhibited solid tumor development. Our study demonstrates that artemisinin caused differential cytotoxic effects depending not only on the concentration and time of exposure but also on the target cells.

Chloroquine exerts antitumor effects on NB4 acute promyelocytic leukemia cells and functions synergistically with arsenic trioxide

“…Cyclin A, CDK2 and CDC25A are critical factors associated with the S phase of the cell cycle (35). CDC25A may activate CDK2, which in turn leads to the activation of the cyclin-CDK complex and causes cell cycle progression (36,37). The present study demonstrated that CQ reduced the expression of CDC25A and CDK2, and increased the expression of cyclin A.…”

Crude extract and solvent fractions of Calystegia soldanella induce G1 and S phase arrest of the cell cycle in HepG2 cells

“…CDC25A is activated by cyclin A/CDK2 complexes. These complexes allow for progression of the cell cycle, and increased expression of CDC25A promotes cell growth (57,58). We have demonstrated that treatment with the C. soldanella 85% aq.…”

More insights into the pharmacological effects of artemisinin

“…Moreover, a recent study from our laboratory demonstrated that artemisinin has a differential effect on cancer cells. In fact, Artemisinin induced lysis on the murin mastocytoma cancer cell line (P815) with IC 50 = 12 μM and on Kidney adeno‐carcinoma cell line of hamsters with IC 50 = 52 μM (Tilaoui, Mouse, Jaafari, & Zyad, ). Furthermore, artemisinin was described to possess an anticancer effect on breast, lung, prostate, colon, leukemia, and other cancer cell types, as summarized in Table .…”

“…Artemisinin has been described to induce apoptosis effects (Chen, Li, Zhang, & Wang, ; Efferth, Giaisi, Merling, Krammer, Li‐Weber ; Hamacher‐Brady et al, ; Tilaoui et al, ; Zheng, Wang, Huang, Luo, & Mi, ), as well as cell cycle arrest, especially at G0/G1 cell cycle transition phase (Tin, Sundar, Tran, et al, ; Willoughby et al, ; Wu et al, ). Multiple lines of evidence suggest that the apoptotic pathway could be due to intra and/or extra‐mitochondrial mode of action and the involvements of iron/heme as well (Efferth et al, ; Lai & Singh, ; Singh & Lai, ; Zhang, Chen, & Gerhard, ).…”