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Lupeol inhibits the proliferation and migration of MDA-MB-231 breast cancer cells via a novel crosstalk mechanism between autophagy and the EMT

机译:Lupeol 通过自噬和 EMT 之间的新型串扰机制抑制 MDA-MB-231 乳腺癌细胞的增殖和迁移

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摘要

Triple-negative breast cancer is the most aggressive type of breast cancer, with a poor prognosis, while effective treatment options are limited. In this study, the anti-tumor effect of lupeol, a natural triterpenoid, toward breast cancer cells and the underlying mechanisms were examined. We firstly predict the primary pathways of lupeol inhibited to TNBC by a network pharmacology approach, which indicated that lupeol may inhibit TNBC via multiple signaling pathways. In addition, experimental data showed that lupeol exhibited outstanding anti-proliferative and anti-metastatic abilities in vitro and in vivo. Additional intrinsic mechanism studies revealed that lupeol might induce autophagy by inhibiting the Akt-mTOR pathway, and activating an autophagy inhibited epithelial–mesenchymal transition (EMT). This study demonstrated that lupeol could inhibit TNBC cells by inducing autophagy, suggesting lupeol as a potential treatment alternative or as a dietary supplement for TNBC, as well as offering novel insights into the anti-cancer effect of lupeol.
机译:三阴性乳腺癌是最具侵袭性的乳腺癌类型,预后不良,而有效的治疗选择有限。本研究探讨了天然三萜类羽扇豆醇对乳腺癌细胞的抗肿瘤作用及其潜在机制。我们首先通过网络药理学方法预测了羽扇豆醇抑制TNBC的主要途径,表明羽扇豆醇可能通过多种信号通路抑制TNBC。此外,实验数据表明,羽扇豆醇在体外和体内均表现出突出的抗增殖和抗转移能力。其他内在机制研究表明,羽扇豆醇可能通过抑制Akt-mTOR通路来诱导自噬,并激活自噬抑制上皮-间充质转化(EMT)。这项研究表明,羽扇豆醇可以通过诱导自噬来抑制TNBC细胞,这表明羽扇豆醇可以作为潜在的治疗选择或作为TNBC的膳食补充剂,并为羽扇豆醇的抗癌作用提供了新的见解。

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