Actinomycin D inhibits cell proliferations and promotes apoptosis in osteosarcoma cells.

Actinomycin D (ActD), a well known transcription inhibitors, has been widely reported to induce cell apoptosis in several types of tumor cells by inhibiting the anti-apoptotic gene transcriptions. However, how ActD affects osteosarcoma cells survival and its molecular mechanism is currently unclear. In the present study, results of proliferation assays and Hoechst stainings suggested that MG63 human osteosarcoma cells showed impaired cell proliferations and significant apoptosis after ActD treatment. Moreover, biochemical results showed that cleaved caspase-3 is gradually increased with the increasing ActD concentrations and treated times. Importantly, results of western blots indicated that protein levels of cyclin factors, such as cyclin A, D1 and E, were all reduced after ActD treatment. And ActD treatments may inhibit mRNA transcription levels of these cyclin factors, which may finally lead to cell cycle arrest and consequently apoptosis. The present study have revealed a novel mechanism by which ActD inhibits osteosarcoma cell proliferations and induces apoptosis, and will provide an useful clue to chemotherapy in future treatment of osteosarcoma.