Background: Despite advances in the treatment of prostate cancer, side effects and the risks of developing
drug resistance require new therapeutic agents. Eupatilin is a secondary metabolite of Artemisia asiatica
and has shown potential anti-tumor activity in some cancers, but its potential in prostate cancer treatment has
not yet been evaluated.
Objective: The aim of the study was to investigate the effectiveness of eupatilin on prostate cancer cell proliferation
Methods: Human prostate cancer PC3 and LNCaP cells were exposed to eupatilin and its efficacy on cell survival
was determined by the MTT test. Apoptosis and cell cycle phases were evaluated by an image-based cytometer.
Cell migration and invasion were evaluated by wound healing and matrigel migration assays; the expression
of mRNA and protein was assessed by RT-qPCR and Western blot, respectively.
Results: Eupatilin time- and dose-dependently reduced the viability of prostate cancer cells. Exposure of PC3
cells to 12.5μM-50μM eupatilin resulted in apoptosis by upregulating the expression of caspase 3, Bax and
cytochrome c. Annexin V assessment also confirmed that eupatilin causes apoptosis. The treatment significantly
upregulated the mRNA expression of p53, p21, and p27, causing cell cycle arrest in the G1 phase. Administration
of eupatilin inhibited migration and invasion of the cells by downregulating the expression of Twist, Slug
and MMP-2, -7. In addition, the agent increased protein expression of tumor suppressor PTEN, while transcription
factor NF-κB expression was reduced.
Conclusion: Eupatilin strongly prevents the proliferation of prostate cancer cells, and suppresses migration and
invasion. Due to its therapeutic potential, the clinical use of eupatilin in prostate cancer should also be supported
by in vivo studies.