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Isochromanoindolenines suppress triple-negative breast cancer cell proliferation partially via inhibiting Akt activation

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收录情况： ◇ SCIE

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机构： [1]Medical Faculty of Kunming University of Science and Technology, Kunming 650500, China. [2]Key Laboratory of Animal Models and Human Disease Mechanisms of the Chinese Academy of Sciences and Yunnan Province, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, 650223, China. [3]Center for Reproductive Medicine, Department of Obstetrics and Gynecology, Peking University Third Hospital, Beijing, 100191, China. [4]College of Chemistry, Fuzhou University, Fuzhou, Fujian 350116, China. [5]Translational Cancer Research Center, Peking University First Hospital, Beijing, 100034, China. [6]KIZ-CUHK Joint Laboratory of Bioresources and Molecular Research in Common Diseases, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, 650223, China. [7]Institute of Translation Medicine, Shenzhen Second People’s Hospital, The First Affiliated Hospital of Shenzhen University, Shenzhen 518035, China.

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关键词： Isochromanoindolenine TNBC cell cycle arrest AKT

摘要：

As the most malignant subtype of breast cancers, triple-negative breast cancer (TNBC) lacks effective targeted therapeutics clinically to date. In this study, one lead compound FZU-0025-065 with isochromanoindolenine scaffold was identified by a cell-based screening. Among nine breast cancer cell lines tested, TNBC are the most sensitive cell lines to FZU-0025-065. FZU-0025-065 inhibits TNBC cell growth in a time- and dosage-dependent manner. FZU-0025-065 suppresses the expression of cell cycle dependent kinase 4 (CDK4), Cyclin D1 and Cyclin B1; meanwhile, elevates the expression of cell cycle dependent kinase inhibitor p21 and p27. Importantly, we found that FZU-0025-065 suppresses AKT activation in a time- and dosage-dependent manner. Over-expression of constitutive active AKT partially rescues FZU-0025-065 induced cell growth inhibition in MDA-MB-468 cells, indicating FZU-0025-065 suppresses TNBC cell growth partially via inhibiting AKT activation. Finally, FZU-0025-065 suppresses TNBC cell growth in a xenograft mouse model. Taken together, our findings suggested that isochromanoindolenine derivative FZU-0025-065 inhibits TNBC via suppressing the AKT signaling and that FZU-0025-065 may be useful for TNBC treatment.

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出版当年[2021]版：

大类 | 2 区生物

小类 | 2 区生化与分子生物学

最新[2025]版：

大类 | 1 区

生物学

小类 | 2 区生化与分子生物学

JCR分区：

出版当年[2020]版：

Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

最新[2023]版：

Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

影响因子： 8.2 最新[2023版] 8.3 最新五年平均 6.582 出版当年[2020版] 6.479 出版当年五年平均 4.858 出版前一年[2019版] 10.75 出版后一年[2021版]

第一作者：

第一作者机构： [1]Medical Faculty of Kunming University of Science and Technology, Kunming 650500, China. [2]Key Laboratory of Animal Models and Human Disease Mechanisms of the Chinese Academy of Sciences and Yunnan Province, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, 650223, China.

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通讯作者：

通讯机构： [2]Key Laboratory of Animal Models and Human Disease Mechanisms of the Chinese Academy of Sciences and Yunnan Province, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, 650223, China. [5]Translational Cancer Research Center, Peking University First Hospital, Beijing, 100034, China. [6]KIZ-CUHK Joint Laboratory of Bioresources and Molecular Research in Common Diseases, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, 650223, China. [7]Institute of Translation Medicine, Shenzhen Second People’s Hospital, The First Affiliated Hospital of Shenzhen University, Shenzhen 518035, China.

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Isochromanoindolenines suppress triple-negative breast cancer cell proliferation partially via inhibiting Akt activation

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