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Polo-like kinase 1 inhibitor BI6727 sensitizes 9L gliosarcoma cells to ionizing irradiation

Journal Article


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Abstract


  • Surgery, chemotherapy and radiotherapy remain as the major treatment strategies for cancers. Some

    agents such as anti-cancer drugs have capacity to enhance the radiation sensitivity of cancer cells at

    G2/M phase, leading to an improved radiotherapeutic efficacy. BI6727 is an ATP-competitive pololike kinase 1 (Plk 1)inhibitor and an anti-cancer drug. Using the radio-resistant 9L rat gliosarcoma

    cells as model, we examined the effect of BI6727 on cell growth and assessed the chemoradiotherapeutic efficiency between 150 kVp conventional irradiation (dose rate of 0.76 Gy min−1

    ) and 66 keV synchrotron x-ray broad beam irradiation (dose rate of 46 Gy s−1). Our studies showed

    that BI6727 significantly caused cell growth arrest at G2/M phase and inhibited 9L cell proliferation

    with EC50 of 58.1 nM. In combinatory treatment, irradiation of BI6727-treated 9L cells with

    synchrotron x-rays at a dose rate of 46 Gy s−1 resulted in significant reduction of the cell survival

    compared to the conventional x-rays at a dose rate of 0.76 Gy min−1. These results indicated that Plk1

    inhibitor BI6727 enhanced radio-sensitization of 9L cells in a dose rate dependent manner. For clinical

    application, irradiation with high dose rate is a promising strategy to improve chemo-radiotherapeutic

    efficacy for gliosarcoma cancer.

Publication Date


  • 2019

Citation


  • Li, N., Engels, E., Davis, J. A., Dipuglia, A., Vogel, S., Valceski, M., Rosenfeld, A. B., Lerch, M. L. F., Corde, S. & Tehei, M. (2019). Polo-like kinase 1 inhibitor BI6727 sensitizes 9L gliosarcoma cells to ionizing irradiation. Biomedical Physics & Engineering Express, 5 067003-1-067003-9.

Scopus Eid


  • 2-s2.0-85076752087

Ro Full-text Url


  • https://ro.uow.edu.au/cgi/viewcontent.cgi?article=4369&context=eispapers1

Ro Metadata Url


  • http://ro.uow.edu.au/eispapers1/3347

Start Page


  • 067003-1

End Page


  • 067003-9

Volume


  • 5

Place Of Publication


  • United Kingdom

Abstract


  • Surgery, chemotherapy and radiotherapy remain as the major treatment strategies for cancers. Some

    agents such as anti-cancer drugs have capacity to enhance the radiation sensitivity of cancer cells at

    G2/M phase, leading to an improved radiotherapeutic efficacy. BI6727 is an ATP-competitive pololike kinase 1 (Plk 1)inhibitor and an anti-cancer drug. Using the radio-resistant 9L rat gliosarcoma

    cells as model, we examined the effect of BI6727 on cell growth and assessed the chemoradiotherapeutic efficiency between 150 kVp conventional irradiation (dose rate of 0.76 Gy min−1

    ) and 66 keV synchrotron x-ray broad beam irradiation (dose rate of 46 Gy s−1). Our studies showed

    that BI6727 significantly caused cell growth arrest at G2/M phase and inhibited 9L cell proliferation

    with EC50 of 58.1 nM. In combinatory treatment, irradiation of BI6727-treated 9L cells with

    synchrotron x-rays at a dose rate of 46 Gy s−1 resulted in significant reduction of the cell survival

    compared to the conventional x-rays at a dose rate of 0.76 Gy min−1. These results indicated that Plk1

    inhibitor BI6727 enhanced radio-sensitization of 9L cells in a dose rate dependent manner. For clinical

    application, irradiation with high dose rate is a promising strategy to improve chemo-radiotherapeutic

    efficacy for gliosarcoma cancer.

Publication Date


  • 2019

Citation


  • Li, N., Engels, E., Davis, J. A., Dipuglia, A., Vogel, S., Valceski, M., Rosenfeld, A. B., Lerch, M. L. F., Corde, S. & Tehei, M. (2019). Polo-like kinase 1 inhibitor BI6727 sensitizes 9L gliosarcoma cells to ionizing irradiation. Biomedical Physics & Engineering Express, 5 067003-1-067003-9.

Scopus Eid


  • 2-s2.0-85076752087

Ro Full-text Url


  • https://ro.uow.edu.au/cgi/viewcontent.cgi?article=4369&context=eispapers1

Ro Metadata Url


  • http://ro.uow.edu.au/eispapers1/3347

Start Page


  • 067003-1

End Page


  • 067003-9

Volume


  • 5

Place Of Publication


  • United Kingdom