Virtual Library

Start Your Search

C. Tabata



Author of

  • +

    P2.01 - Poster Session 2 - Cancer Biology (ID 145)

    • Event: WCLC 2013
    • Type: Poster Session
    • Track: Biology
    • Presentations: 1
    • +

      P2.01-021 - AMP Converted from Intracellularly Transported Adenosine Upregulates p53 Expression to Induce Malignant Pleural Mesothelioma Cell Apoptosis (ID 1174)

      09:30 - 09:30  |  Author(s): C. Tabata

      • Abstract

      Background
      The present study investigated adenosine-induced apoptosis in human malignant pleural mesothelioma cells.

      Methods
      MTT assay, TUNEL staining, flow cytometry using propidium iodide and annexin V-FITC, real-time RT-PCR, Western blotting, and assay of caspase-3, -8, and -9 activities were carried out using malignant pleural mesothelioma cell lines such as NCI-H28, NCI-H2052, NCI-H2452, and MSTO-211H cells, and P53 or A3 adenosine receptor was knocked-down by transfecting each siRNA into cells.

      Results
      Adenosine induced apoptosis in all the malignant pleural mesothelioma cells used here, independently of caspase activation. The adenosine effect was prevented by the adenosine transporter inhibitor dipyridamole, the adenosine kinase inhibitor ABT-702, or the A3 adenosine receptor inhibitor MRS1191. Adenosine upregulated expression of the p53 mRNA and protein, that is abolished by ABT-702, but not by knocking-down A3 adenosine receptor. Adenosine-induced apoptosis in NCI-H28 cells was significantly inhibited by knocking-down p53 and in part by knocking-down A3 adenosine receptor.

      Conclusion
      The results of the present study show that AMP converted from intracellularly transported adenosine upregulates p53 expression to induce caspase-independent apoptosis in malignant pleural mesothelioma cells and that A3 adenosine receptor also participates partially in the apoptosis by the different mechanism.