Arsenic Trioxide Suppresses Tumor Growth through Antiangiogenesis via Notch Signaling Blockade in Small-Cell Lung Cancer.

Small-cell lung cancer (SCLC) is a highly malignant type of lung cancer with no effective second-line chemotherapy drugs. Arsenic trioxide (As2O3) was reported to exert antiangiogenesis activities against lung cancer and induce poor development of vessel structures, similar to the effect observed fo...

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Publicado en:BioMed Research International pp. 1 - 10
Autores principales: Yang, Meng-Hang, Chang, Ke-Jie, Li, Bing, Chen, Wan-Sheng
Formato: pictorial research tables/charts Journal Article
Publicado: Wiley-Blackwell 4/10/2019
Acceso en línea:Ver este registro en EBSCOhost
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      dt: 4/10/2019
      pid: 480
      pub: Wiley-Blackwell
      place: Malden, Massachusetts
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        10.1155/2019/4647252
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        atl: Arsenic Trioxide Suppresses Tumor Growth through Antiangiogenesis via Notch Signaling Blockade in Small-Cell Lung Cancer.
      aug:
        au:
          Yang, Meng-Hang
          Chang, Ke-Jie
          Li, Bing
          Chen, Wan-Sheng
        affil: Department of Respiratory and Critical Care Medicine, Changzheng Hospital, Second Military Medical University, Shanghai 200003, China
      sug:
        subj:
          Arsenicals Pharmacodynamics
          Cell Line, Tumor Drug Effects
          Signal Transduction Drug Effects
          Neovascularization, Physiologic Drug Effects
          Membrane Proteins Drug Effects
          Carcinoma, Non-Small-Cell Lung Drug Therapy
          Human
          Transcription Factors Drug Effects
          Blood Vessels Drug Effects
          In Vivo Studies
          Gene Expression Drug Effects
          Umbilical Veins Drug Effects
          Epithelial Cells Drug Effects
      ab: Small-cell lung cancer (SCLC) is a highly malignant type of lung cancer with no effective second-line chemotherapy drugs. Arsenic trioxide (As2O3) was reported to exert antiangiogenesis activities against lung cancer and induce poor development of vessel structures, similar to the effect observed following the blockade of Notch signaling. However, there are no direct evidences on the inhibitory effects of As2O3 on tumor growth and angiogenesis via blockade of Notch signaling in SCLC. Here, we found that As2O3 significantly inhibited the tumor growth and angiogenesis in SCLC and reduced the microvessel density. As2O3 disturbed the morphological development of tumor vessels and downregulated the protein levels of delta-like canonical Notch ligand 4 (Dll4), Notch1, and Hes1 in vivo. DAPT, a Notch signaling inhibitor, exerted similar effects in SCLC. We found that both As2O3 treatment and Notch1 expression knockdown resulted in the interruption of tube formation by human umbilical vein endothelial cells (HUVECs) on Matrigel. As2O3 had no effects on Dll4 level in HUVECs but significantly inhibited the expression of Notch1 and its downstream gene Hes1 regardless of Dll4 overexpression or Notch1 knockdown. These findings suggest that the antitumor activity of As2O3 in SCLC was mediated via its antiangiogenic effect through the blockade of Notch signaling, probably owing to Notch1 targeting.
      pubtype: Academic Journal
      doctype:
        pictorial
        research
        tables/charts
        Journal Article
      ougenre: Article
    language: English
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