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首页> 外文期刊>Frontiers in Pharmacology >Mechanistic Study of Bakuchiol-Induced Anti-breast Cancer Stem Cell and in Vivo Anti-metastasis Effects
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Mechanistic Study of Bakuchiol-Induced Anti-breast Cancer Stem Cell and in Vivo Anti-metastasis Effects

机译：补骨脂酚诱导的抗乳腺癌干细胞的机制研究及体内抗抗转移作用

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Cancer stem cells are involved in cancer establishment, progression, and resistance to current treatments. We demonstrated the in vitro and in vivo anti-breast cancer effect of bakuchiol in a previous study. However, the ability of bakuchiol to target breast cancer stem cells (BCSCs) and inhibit breast cancer metastasis remains unknown. In the current study, we used the cell surface markers CD44 and CD24 to distinguish BCSCs from MCF-7 cells. Bakuchiol inhibited mammosphere formation and aldehyde dehydrogenase activity in BCSCs. Moreover, bakuchiol induced apoptosis and suppressed the mitochondrial membrane potential of BCSCs. Bakuchiol upregulated the expression levels of pro-apoptotic genes, BNIP3 and DAPK2. Bakuchiol induced oxidative stress and altered lipogenesis in BCSCs. In zebrafish xenografts, bakuchiol inhibited breast cancer cell metastasis in vivo. In addition, bakuchiol altered the expression levels of metastasis-related genes through upregulating CK18 and downregulating Notch3, FASN, TGFBR1, and ACVR1B. Our study provides evidence for the anti-breast cancer potential of bakuchiol.
机译：癌症干细胞参与癌症的建立，发展和对当前治疗的抵抗力。在先前的研究中，我们证明了补骨脂酚的体外和体内抗乳腺癌作用。然而，爆裂酚靶向乳腺癌干细胞（BCSCs）和抑制乳腺癌转移的能力仍然未知。在当前的研究中，我们使用细胞表面标记CD44和CD24来区分BCSC和MCF-7细胞。补骨脂酚可抑制BCSC中的乳球形成和醛脱氢酶活性。此外，补骨脂酚诱导细胞凋亡并抑制BCSCs的线粒体膜电位。补骨脂酚上调凋亡前基因BNIP3和DAPK2的表达水平。幕果酚在BCSC中诱导氧化应激并改变脂肪形成。在斑马鱼异种移植物中，补骨脂酚在体内抑制乳腺癌细胞转移。此外，补骨脂酚通过上调CK18和下调Notch3，FASN，TGFBR1和ACVR1B来改变转移相关基因的表达水平。我们的研究为补骨脂的抗乳腺癌潜力提供了证据。

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