Pelargonidin induces antitumor effects in human osteosarcoma cells via autophagy induction, loss of mitochondrial membrane potential, G2/M cell cycle arrest and downregulation of PI3K/AKT signalling pathway.

PURPOSE

Osteosarcoma is the most common type of primary malignancy of bone in children and adults. The treatment options for osteosarcoma are limited and are associated with a number of drawbacks. Therefore there is an urgent need to look for more efficient options for the treatment of this disease. Flavonoids have been considered as important anticancer agents due to their efficacy and lower cytotoxicity. In the present study we evaluated the anticancer effects of pelargonidin in U2OS osteosarcoma cell line.

METHODS

Cell viability was assessed by MTT assay. Reactive oxygen species (ROS), mitochondrial membrane potential (MMP) and cell cycle analysis was done by flow cytometry. Expression of proteins was examined by western blotting.

RESULTS

Pelargonidin exhibited significant anticancer effects on osteosarcoma U2OS cell line with an IC50 of 15 μM. The anticancer effects of pelargonidin were due to induction of autophagy as evidenced from the expression of LC3-I, LC-3II and Beclin-1. Moreover, pelargonidin triggered ROSinduced reduction in MMP and triggered G2/M cell cycle arrest. In addition, pelargonidin inhibited the expression of p-PI3K and p-AKT in a concentration-dependent manner.

CONCLUSIONS

Taken together, these results indicated that pelargonidin may prove a potential lead drug for the treatment of osteosarcoma.