Antrodin C was obtained from Taiwanofungus camphoratus mycelia. The inhibition effect of
antrodin C on A549
lung adenocarcinoma cells was evaluated by plate clone formation, wound healing, cell cycle, activated
caspase-3, Bax, P53, Bcl-2, and RAPR activities as well as
reactive oxygen species release. Plate clone formation assay revealed that
antrodin C could significantly inhibit the viability of A549 cells in vitro. Wound healing assay revealed that cell migration was inhibited by exposure to
antrodin C at concentrations of 50 and 80 μg/mL. Flow cytometry revealed that
antrodin C increased the percentages of cells in the G0/G1 phase at concentrations of 50 and 80 μg/mL and the apoptosis was related to upregulation of
caspase-3, Bax, P53 expression, downregulation of Bcl-2, RAPR expression, and the release of
reactive oxygen species in the A549 cells. CQ or RAPA could significantly promote or inhibit the inhibition effect on A549 proliferation induced by
antrodin C, which suggests that the autophagy played a cytoprotective role on inhibition proliferation of A549 induced by
antrodin C. These results indicated that the combination of pro-apoptosis agents and anti-autophagy agents may be a useful strategy in enhancing the anticancer efficacy in
non-small cell lung cancer.