Acute promyelocytic leukemia (APL) remains a challenge to cure due to the side effects of cytotoxic chemotherapy and drug resistance. The present study demonstrated that vernodalol, an active compound isolated from Centratherum anthelminticum, suppresses APL cell proliferation and induces cell cycle arrest in the G2/M phase through the upregulation of p21 and cell division cycle 25. In addition, vernodalol induced cellular apoptosis via the mitochondrial pathway as observed by the cleavage of caspase-9 as well as the release of cytochrome c and Smac/DIABLO into the cytosol. A mechanistic study revealed that vernodalol may exert its antitumor activity through the suppression of phosphoinositide 3-kinase/protein kinase B/mechanistic target of rapamycin signaling. In conclusion, vernodalol may be developed as a potential therapeutic compound for the treatment of APL.
Keywords: acute promyelocytic leukemia; apoptosis; cell cycle; phosphoinositide 3-kinase/protein kinase B/mechanistic target of rapamycin; vernodalol.