Crowberry inhibits cell proliferation and migration through a molecular mechanism that includes inhibition of DEK and Akt signaling in cholangiocarcinoma.
Crowberry inhibits cell proliferation and migration through a molecular mechanism that includes inhibition of DEK and Akt signaling in cholangiocarcinoma.
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岩高兰通过抑制胆管癌中 DEK 和 Akt 信号传导的分子机制抑制细胞增殖和迁移
DOI：
10.1186/s13020-022-00623-6
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发表时间：
2022-06-13
期刊：
影响因子：
4.9
通讯作者：
Ren, Xiangshan
中科院分区：
文献类型：
--
作者：
Wang, Xue;Zhou, Xuebing;Zhang, Ludan;Zhang, Xin;Yang, Chunyu;Piao, Yingshi;Zhao, Jinhua;Jin, Lili;Jin, Guihua;An, Renbo;Ren, Xiangshan
胆管癌（CCA）是一种罕见的胆管腺癌，临床预后不良。岩高兰是一种草药，用于控制炎症性疾病和重建抗氧化酶活性。尽管岩高兰对多种肿瘤和疾病显示出显着的治疗功效，但其在 CCA 中的抗癌作用和具体分子机制尚不清楚。本研究旨在表征岩高兰对 CCA 细胞行为的影响。通过高效液相色谱 (HPLC) 和 HPLC-串联质谱法对岩高兰提取物的化学成分进行定性分析。进行 MTT、集落形成和 EdU 测定来测量细胞增殖。通过伤口愈合和迁移测定评估岩高兰治疗对 CCA 细胞迁移的影响。此外，进行Hoechst染色测定和流式细胞术来评估细胞凋亡率。 Western blotting 用于评估与细胞凋亡、Akt 信号通路和上皮间质转化相关的关键因子的蛋白表达水平。建立异种移植模型并进行免疫组织化学和H&E染色以评估岩高兰的体内抗肿瘤作用。 Crowberry 以剂量依赖性方式明显抑制 CCA 细胞增殖和迁移，并在体外诱导细胞凋亡。 Crowberry 在体外通过调节 DEK 灭活 PI3K/Akt 信号通路，并通过下调异种移植模型中的 DEK 表达显着抑制肿瘤生长。 Crowberry 通过一种分子机制抑制 CCA 细胞增殖和迁移，包括体外和体内抑制 DEK 和 Akt 信号通路抑制。在线版本包含可在 10.1186/s13020-022-00623-6 获取的补充材料。岩高兰改变了 PI3K/Akt 信号通路中关键介质的表达水平。岩高兰改变了 PI3K/Akt 信号通路中关键介质的表达水平。岩高兰在体内和体外均抑制原癌基因 DEK 的表达。 Crowberry 通过一种分子机制抑制 CCA 进展和迁移，其中包括体内和体外抑制 DEK 和 Akt 信号通路。在线版本包含可在 10.1186/s13020-022-00623-6 获取的补充材料。
Cholangiocarcinoma (CCA) is a rare biliary adenocarcinoma related to poor clinical prognosis. Crowberry is an herbal medicine used to control inflammatory diseases and reestablish antioxidant enzyme activity. Although crowberry shows significant therapeutic efficacy in various tumors and diseases, its anticancer effects and specific molecular mechanisms in CCA are poorly understood. This study was conducted to characterize crowberry effects on CCA cells behavior. The chemical profiles of crowberry extract was qualitatively analyzed by high-performance liquid chromatography (HPLC) and HPLC–tandem mass spectrometry. MTT, colony formation and EdU assays were performed to measure cell proliferation. The effect of crowberry treatment on CCA cell migration was assessed by wound healing and migration assays. Moreover, Hoechst staining assay and flow cytometry were performed to assess the cell apoptosis rate. Western blotting was used to assess the protein expression levels of key factors associated with apoptosis, the Akt signaling pathway, and the epithelial-mesenchymal transition. A xenograft model was established and immunohistochemical and H&E staining was performed to assess crowberry antitumor effects in vivo. Crowberry clearly inhibited CCA cells proliferation and migration in a dose-dependent manner and induced apoptosis in vitro. Crowberry inactivated the PI3K/Akt signaling pathway by regulating DEK in vitro and significantly inhibited tumor growth by downregulating the DEK expression in xenograft models. Crowberry inhibits CCA cells proliferation and migration through a molecular mechanism that includes inhibition of DEK and Akt signaling pathway inhibition in vitro and in vivo. The online version contains supplementary material available at 10.1186/s13020-022-00623-6. Crowberry alterd expression levels of key mediators in PI3K/Akt signaling pathway. Crowberry alterd expression levels of key mediators in PI3K/Akt signaling pathway. Crowberry suppressed the expression of the proto-oncogene DEK in vivo and in vitro. Crowberry inhibited CCA progression and migration through a molecular mechanism that includes inhibition of DEK and the Akt signaling pathway in vivo and in vitro. The online version contains supplementary material available at 10.1186/s13020-022-00623-6.
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影响因子：
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作者：
Nye J;Melters DP;Dalal Y
通讯作者：
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影响因子：
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DOI：
10.1124/jpet.119.263202
发表时间：
2020-05-01
影响因子：
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作者：
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通讯作者：
Ren, Xiangshan
影响因子：
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