b -Escin inhibits the proliferation of osteosarcoma cells via blocking the PI3K/Akt pathway

b -Escin exhibits anticancer e ff ects on a panel of established cancer cells. However, the e ff ects of b -escin on human osteosarcoma (OS) are still unknown. The aim of the present study was to investigate whether b escin was e ff ective against OS both in vivo and in vitro . Our results showed that b -escin induced dose-and time-dependent e ff ects against MG-63, OS732, U-2OS, HOS and SAOS-2 cell proliferation. b -Escin also exhibited excellent anti-proliferative and pro-apoptotic e ff ects in an established OS xenograft model. b -Escin and cytotoxic drugs, including cisplatin, methotrexate (MTX), doxorubicin (Dox) and ifosfamide (Ifos), synergistically inhibited proliferation of MG-63 and OS732 cells in vitro . Moreover, b escin induced apoptotic death, activated caspase-3, caspase-8 and caspase-9, and regulated expression of Bax and Bcl-2 in MG-63 cells. In addition, our results showed that b -escin treatment reduced expression of p-PI3K, p-Akt and p-mTOR both in MG-63 cells and in an MG-63 xenograft OS model. Interestingly, SC79, which is an Akt activator, inhibited the anti-proliferative e ff ects of b -escin on MG-63 cells. Taken together, our data support the conclusion that b -escin e ff ectively inhibits OS proliferation both in vivo and in vitro . The inhibitory e ff ect of b -escin, at least in part, is due to the inactivation of the PI3K/Akt signalling pathway.

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