Author of

• 10497

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  P1.01 - Poster Session 1 - Cancer Biology (ID 143)

  • Event: WCLC 2013
  • Type: Poster Session
  • Track: Biology
  • Presentations: 1
  • Moderators:
  • Coordinates: 10/28/2013, 09:30 - 16:30, Exhibit Hall, Ground Level

  • 10522

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    P1.01-025 - Apoptosis-Related Gene Transcription in Human A549 Lung Cancer Cells via A₃Adenosine Receptor (ID 2157)

    15:06 - 15:20  |  Author(s): T. Terada
    • Abstract

    Background
    Extracellular adenosine induces apoptosis in a variety of cancer cells via diverse signaling pathways. The present study investigated the mechanism underlying adenosine-induced apoptosis in A549 human lung cancer cells.

    Methods
    MTT assay, TUNEL staining, flow cytometry using propidium iodide and annexin V-FITC, real-time RTPCR, Western blotting, monitoring of mitochondrial membrane potentials, and assay of caspase-3, -8, and -9 activities were carried out in A549 cells, and the siRNA to silence the A~3 ~adenosine receptortargeted gene was constructed.

    Results
    Extracellular adenosine induces A549 cell apoptosis in a concentration(0.01-10 mM)-dependent manner, and the effect was inhibited by the A~3~ adenosine receptor inhibitor MRS1191 or knocking-down A~3~ adenosine receptor. Like adenosine, the A~3~ adenosine receptor agonist 2-Cl-IB-MECA also induced A549 cell apoptosis. Adenosine increased expression of mRNAs for Puma, Bax, and Bad, disrupted mitochondrial membrane potentials, and activated caspase-3 and -9 in A549 cells, and those adenosine effects were also suppressed by knocking-down A~3~ adenosine receptor.

    Conclusion
    Adenosine induces A549 cell apoptosis by upregulating expression of Bax, Bad, and Puma, to disrupt mitochondrial membrane potentials and to activate caspase-9 followed by the effector caspase-3, via A~3~ adenosine receptor.

• 12364

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  P3.01 - Poster Session 3 - Cancer Biology (ID 147)

  • Event: WCLC 2013
  • Type: Poster Session
  • Track: Biology
  • Presentations: 1
  • Moderators:
  • Coordinates: 10/30/2013, 09:30 - 16:30, Exhibit Hall, Ground Level

  • 12385

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    P3.01-021 - A3 Adenosine Receptor-Mediated p53- Dependent Apoptosis in Lu-65 Human Lung Cancer Cells (ID 1208)

    09:30 - 09:30  |  Author(s): T. Terada
    • Abstract

    Background
    A3 adenosine receptor mediates apoptosis in cancer cells via diverse signaling pathways. The present study examined A3 adenosine receptor-mediated apoptosis in Lu-65 cells, a human giant cell lung carcinoma cell line.

    Methods
    MTT assay, TUNEL staining, real-time RT-PCR, Western blotting, and assay of caspase-3, -8, and -9 activities were carried out in Lu-65 cells, and A3 adenosine receptor or p53 was knocked-down by transfecting each siRNA into cells.

    Results
    Extracellular adenosine induces Lu-65 cell apoptosis in a concentration (0.01-10 mM)-dependent manner, and the effect was inhibited by the A3 adenosine receptor inhibitor MRS1191 or by knocking-down A3 adenosine receptor or p53. Like adenosine, the A3 adenosine receptor agonist 2-Cl-IB-MECA also induced Lu-65 cell apoptosis. Adenosine upregulated expression of p53 and Noxa mRNAs and activated caspase-3 and -9, but not caspase-8. Those adenosine effects were still inhibited by knocking- down A3 adenosine receptor or p53.

    Conclusion
    The results of the present study show that adenosine upregulates p53 expression via A3 adenosine receptor, to promote p53-dependent Noxa gene transcription, causing activation of caspase-9 and the effector caspase-3 to induce Lu-65 cell apoptosis.