苍术内酯 I 通过抑制 Notch 通路衰减胃癌干细胞特性。
Atractylenolide I-mediated Notch pathway inhibition attenuates gastric cancer stem cell traits.
机构信息
State Key Laboratory of Bioreactor Engineering & Shanghai Key Laboratory of New Drug Design, School of Pharmacy, East China University of Science and Technology, #268, 130 Meilong Road, Shanghai 200237, PR China.
State Key Laboratory of Bioreactor Engineering & Shanghai Key Laboratory of New Drug Design, School of Pharmacy, East China University of Science and Technology, #268, 130 Meilong Road, Shanghai 200237, PR China.
出版信息
Biochem Biophys Res Commun. 2014 Jul 18;450(1):353-9. doi: 10.1016/j.bbrc.2014.05.110. Epub 2014 Jun 2.
Atractylenolide I (AT-I), one of the main naturally occurring compounds of Rhizoma Atractylodis Macrocephalae, has remarkable anti-cancer effects on various cancers. However, its effects on the treatment of gastric cancer remain unclear. Via multiple cellular and molecular approaches, we demonstrated that AT-I could potently inhibit cancer cell proliferation and induce apoptosis through inactivating Notch pathway. AT-I treatment led to the reduction of expressions of Notch1, Jagged1, and its downstream Hes1/ Hey1. Our results showed that AT-I inhibited the self-renewal capacity of gastric stem-like cells (GCSLCs) by suppression of their sphere formation capacity and cell viability. AT-I attenuated gastric cancer stem cell (GCSC) traits partly through inactivating Notch1, leading to reducing the expressions of its downstream target Hes1, Hey1 and CD44 in vitro. Collectively, our results suggest that AT-I might develop as a potential therapeutic drug for the treatment of gastric cancer.
白术内酯 I（AT-I）是白术的主要天然化合物之一，对多种癌症具有显著的抗癌作用。然而，其在胃癌治疗中的作用尚不清楚。通过多种细胞和分子方法，我们证明 AT-I 可以通过抑制 Notch 通路强烈抑制癌细胞增殖并诱导细胞凋亡。AT-I 处理导致 Notch1、Jagged1 及其下游 Hes1/Hey1 的表达减少。我们的结果表明，AT-I 通过抑制其球体形成能力和细胞活力来抑制胃干样细胞（GCSLC）的自我更新能力。AT-I 通过抑制 Notch1 部分减弱胃肿瘤干细胞（GCSC）的特征，导致其下游靶标 Hes1、Hey1 和 CD44 的表达减少。总之，我们的研究结果表明，AT-I 可能成为治疗胃癌的潜在治疗药物。
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