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首页> 外文期刊>Evidence-based complementary and alternative medicine: eCAM >Ganoderma tsugae Induces S Phase Arrest and Apoptosis in Doxorubicin-Resistant Lung Adenocarcinoma H23/0.3 Cells via Modulation of the PI3K/Akt Signaling Pathway
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Ganoderma tsugae Induces S Phase Arrest and Apoptosis in Doxorubicin-Resistant Lung Adenocarcinoma H23/0.3 Cells via Modulation of the PI3K/Akt Signaling Pathway

机译:tsugae灵芝通过调节PI3K / Akt信号通路在耐阿霉素的肺腺癌H23 / 0.3细胞中诱导S期阻滞和凋亡。

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摘要

Ganoderma tsugae (GT) is a traditional Chinese medicine that exhibits significant antitumor activities against many types of cancer. This study investigated the molecular mechanism by which GT suppresses the growth of doxorubicin-resistant lung adenocarcinoma H23/0.3 cells. Our results reveal that GT inhibits the viability of H23/0.3 cells in vitro and in vivo and sensitizes the growth suppression effect of doxorubicin on H23/0.3 cells. The data also show that GT induces S phase arrest by interfering with the protein expression of cyclin A, cyclin E, CDK2, and CDC25A. Furthermore, GT induces cellular apoptosis via induction of a mitochondria/caspase pathway. In addition, we also demonstrate that the suppression of cell proliferation by GT is through down-regulation of the PI3K/Akt signaling pathway. In conclusion, this study suggests that GT may be a useful adjuvant therapeutic agent in the treatment of lung cancer.
机译:tsugae灵芝(GT)是一种传统中药,对多种类型的癌症均表现出显着的抗肿瘤活性。这项研究调查了GT抑制耐药阿霉素肺腺癌H23 / 0.3细胞生长的分子机制。我们的结果表明,GT在体外和体内均抑制H23 / 0.3细胞的活力,并使阿霉素对H23 / 0.3细胞的生长抑制作用敏感。数据还显示,GT通过干扰细胞周期蛋白A,细胞周期蛋白E,CDK2和CDC25A的蛋白质表达来诱导S期停滞。此外,GT通过线粒体/胱天蛋白酶途径的诱导来诱导细胞凋亡。此外,我们还证明了GT对细胞增殖的抑制作用是通过PI3K / Akt信号通路的下调来实现的。总之,这项研究表明GT可能是治疗肺癌的有用辅助治疗剂。

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