A549电池
细胞凋亡
自噬
下调和上调
细胞周期
活性氧
化学
流式细胞术
药理学
活力测定
细胞生长
生物
细胞生物学
分子生物学
生物化学
基因
作者
Wenhan Wang,Hairui Yang,Jing Deng,Lina Zhu,Yan Yang,Zhendong Liu,Jingsong Zhang,Chuanhong Tang,Zhong Zhang,Haining Zhuang,Henan Zhang,Wei Jia
标识
DOI:10.1615/intjmedmushrooms.2019025901
摘要
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.
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