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RAD51 Is a Selective DNA Repair Target to Radiosensitize Glioma Stem Cells

Research output: Contribution to Journal/Magazine › Journal article › peer-review

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RAD51 Is a Selective DNA Repair Target to Radiosensitize Glioma Stem Cells. / King, Harry O.; Brend, Tim; Payne, Helen L. et al.
In: Stem Cell Reports, Vol. 8, No. 1, 10.01.2017, p. 125-139.

Research output: Contribution to Journal/Magazine › Journal article › peer-review

Harvard

King, HO, Brend, T, Payne, HL, Wright, A, Ward, TA, Patel, K, Egnuni, T, Stead, LF, Patel, A, Wurdak, H & Short, SC 2017, 'RAD51 Is a Selective DNA Repair Target to Radiosensitize Glioma Stem Cells', Stem Cell Reports, vol. 8, no. 1, pp. 125-139. https://doi.org/10.1016/j.stemcr.2016.12.005

APA

King, H. O., Brend, T., Payne, H. L., Wright, A., Ward, T. A., Patel, K., Egnuni, T., Stead, L. F., Patel, A., Wurdak, H., & Short, S. C. (2017). RAD51 Is a Selective DNA Repair Target to Radiosensitize Glioma Stem Cells. Stem Cell Reports, 8(1), 125-139. https://doi.org/10.1016/j.stemcr.2016.12.005

Vancouver

King HO, Brend T, Payne HL, Wright A, Ward TA, Patel K et al. RAD51 Is a Selective DNA Repair Target to Radiosensitize Glioma Stem Cells. Stem Cell Reports. 2017 Jan 10;8(1):125-139. doi: 10.1016/j.stemcr.2016.12.005

Author

King, Harry O. ; Brend, Tim ; Payne, Helen L. et al. / RAD51 Is a Selective DNA Repair Target to Radiosensitize Glioma Stem Cells. In: Stem Cell Reports. 2017 ; Vol. 8, No. 1. pp. 125-139.

Bibtex

@article{dc6dd8dc0a9b4a0ebc2e0646c675bbe1,
title = "RAD51 Is a Selective DNA Repair Target to Radiosensitize Glioma Stem Cells",
abstract = "Patients with glioblastoma die from local relapse despite surgery and high-dose radiotherapy. Resistance to radiotherapy is thought to be due to efficient DNA double-strand break (DSB) repair in stem-like cells able to survive DNA damage and repopulate the tumor. We used clinical samples and patient-derived glioblastoma stem cells (GSCs) to confirm that the DSB repair protein RAD51 is highly expressed in GSCs, which are reliant on RAD51-dependent DSB repair after radiation. RAD51 expression and RAD51 foci numbers fall when these cells move toward astrocytic differentiation. In GSCs, the small-molecule RAD51 inhibitors RI-1 and B02 prevent RAD51 focus formation, reduce DNA DSB repair, and cause significant radiosensitization. We further demonstrate that treatment with these agents combined with radiation promotes loss of stem cells defined by SOX2 expression. This indicates that RAD51-dependent repair represents an effective and specific target in GSCs.",
keywords = "glioblastoma, glioma stem cell, RAD51, radiosensitization",
author = "King, {Harry O.} and Tim Brend and Payne, {Helen L.} and Alexander Wright and Ward, {Thomas A.} and Karan Patel and Teklu Egnuni and Stead, {Lucy F.} and Anjana Patel and Heiko Wurdak and Short, {Susan C.}",
year = "2017",
month = jan,
day = "10",
doi = "10.1016/j.stemcr.2016.12.005",
language = "English",
volume = "8",
pages = "125--139",
journal = "Stem Cell Reports",
issn = "2213-6711",
publisher = "Cell Press",
number = "1",

}

RIS

TY - JOUR

T1 - RAD51 Is a Selective DNA Repair Target to Radiosensitize Glioma Stem Cells

AU - King, Harry O.

AU - Brend, Tim

AU - Payne, Helen L.

AU - Wright, Alexander

AU - Ward, Thomas A.

AU - Patel, Karan

AU - Egnuni, Teklu

AU - Stead, Lucy F.

AU - Patel, Anjana

AU - Wurdak, Heiko

AU - Short, Susan C.

PY - 2017/1/10

Y1 - 2017/1/10

N2 - Patients with glioblastoma die from local relapse despite surgery and high-dose radiotherapy. Resistance to radiotherapy is thought to be due to efficient DNA double-strand break (DSB) repair in stem-like cells able to survive DNA damage and repopulate the tumor. We used clinical samples and patient-derived glioblastoma stem cells (GSCs) to confirm that the DSB repair protein RAD51 is highly expressed in GSCs, which are reliant on RAD51-dependent DSB repair after radiation. RAD51 expression and RAD51 foci numbers fall when these cells move toward astrocytic differentiation. In GSCs, the small-molecule RAD51 inhibitors RI-1 and B02 prevent RAD51 focus formation, reduce DNA DSB repair, and cause significant radiosensitization. We further demonstrate that treatment with these agents combined with radiation promotes loss of stem cells defined by SOX2 expression. This indicates that RAD51-dependent repair represents an effective and specific target in GSCs.

AB - Patients with glioblastoma die from local relapse despite surgery and high-dose radiotherapy. Resistance to radiotherapy is thought to be due to efficient DNA double-strand break (DSB) repair in stem-like cells able to survive DNA damage and repopulate the tumor. We used clinical samples and patient-derived glioblastoma stem cells (GSCs) to confirm that the DSB repair protein RAD51 is highly expressed in GSCs, which are reliant on RAD51-dependent DSB repair after radiation. RAD51 expression and RAD51 foci numbers fall when these cells move toward astrocytic differentiation. In GSCs, the small-molecule RAD51 inhibitors RI-1 and B02 prevent RAD51 focus formation, reduce DNA DSB repair, and cause significant radiosensitization. We further demonstrate that treatment with these agents combined with radiation promotes loss of stem cells defined by SOX2 expression. This indicates that RAD51-dependent repair represents an effective and specific target in GSCs.

KW - glioblastoma

KW - glioma stem cell

KW - RAD51

KW - radiosensitization

U2 - 10.1016/j.stemcr.2016.12.005

DO - 10.1016/j.stemcr.2016.12.005

M3 - Journal article

C2 - 28076755

AN - SCOPUS:85009115425

VL - 8

SP - 125

EP - 139

JO - Stem Cell Reports

JF - Stem Cell Reports

SN - 2213-6711

IS - 1

ER -