Artemisinin, a plant-derived anti-malarial drug with relatively low toxicity on normal cells in humans, has selective anti-cancer activities in various types of cancers, both in vitro and in vivo. In the present study, we have investigated the anti-cancer effects of artemisinin in human cervical cancer cells, with special emphasis on its role in inducing apoptosis and repressing cell proliferation by inhibiting the telomerase subunits, the ERα which is essential for maintenance of the cervix, and downstream components like VEGF, which is known to activate angiogenesis.

Effects of artemisinin on apoptosis of ME-180 cells were measured by flow cytometry, DAPI and annexin V staining. Expression of genes and proteins related to cell proliferation and apoptosis were quantified both at the transcriptional and translational levels by semi-quantitative RT-PCR and western blot analysis, respectively.

Our findings demonstrated that artemisinin significantly down regulated the expression of ERα and its downstream component, VEGF. Anti-proliferative activity was also supported by decreased telomerase activity and reduced expression of hTR and hTERT subunits. Additionally, artemisinin reduced expression of the HPV-39 viral E6 and E7 components. Artemisinin-induced apoptosis was confirmed by FACS, nuclear chromatin condensation, annexin V staining. Increased expression of p53 with concomitant decrease in expression of the p53 inhibitor Mdm2, further supported that artemisinin-induced apoptosis was p53-dependent.

The results clearly indicate that artemisinin induces anti-proliferative and pro-apoptotic effects in HPV-39 infected ME-180 cells, and warrants further trial as an effective anti-cancer drug. This article is protected by copyright. All rights reserved.