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HPV-positive HNSCC cell lines but not primary human fibroblasts are radiosensitized by the inhibition of Chk1

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HPV-positive HNSCC cell lines but not primary human fibroblasts are radiosensitized by the inhibition of Chk1. / Busch, Chia-Jung; Kriegs, Malte; Laban, Simon; Tribius, Silke; Knecht, Rainald; Petersen, Cordula; Dikomey, Ekkehard; Rieckmann, Thorsten.

in: RADIOTHER ONCOL, Jahrgang 108, Nr. 3, 01.09.2013, S. 495-9.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Busch, C-J, Kriegs, M, Laban, S, Tribius, S, Knecht, R, Petersen, C, Dikomey, E & Rieckmann, T 2013, 'HPV-positive HNSCC cell lines but not primary human fibroblasts are radiosensitized by the inhibition of Chk1', RADIOTHER ONCOL, Jg. 108, Nr. 3, S. 495-9. https://doi.org/10.1016/j.radonc.2013.06.035

APA

Busch, C-J., Kriegs, M., Laban, S., Tribius, S., Knecht, R., Petersen, C., Dikomey, E., & Rieckmann, T. (2013). HPV-positive HNSCC cell lines but not primary human fibroblasts are radiosensitized by the inhibition of Chk1. RADIOTHER ONCOL, 108(3), 495-9. https://doi.org/10.1016/j.radonc.2013.06.035

Vancouver

Busch C-J, Kriegs M, Laban S, Tribius S, Knecht R, Petersen C et al. HPV-positive HNSCC cell lines but not primary human fibroblasts are radiosensitized by the inhibition of Chk1. RADIOTHER ONCOL. 2013 Sep 1;108(3):495-9. https://doi.org/10.1016/j.radonc.2013.06.035

Bibtex

@article{398ee8b0f0e2449f9d63a9a1edc8498b,
title = "HPV-positive HNSCC cell lines but not primary human fibroblasts are radiosensitized by the inhibition of Chk1",
abstract = "PURPOSE: Despite the comparably high cure rates observed for HPV-positive HNSCC, there is still a great need for specific tumor radiosensitization due to the often severe side effects resulting from intense radiochemotherapy. We recently demonstrated that HPV-positive HNSCC cell lines are characterized by a defect in DNA double-strand break repair associated with a pronounced G2-arrest. Here we tested whether abrogation of this radiation-induced G2-arrest by the inhibition of Chk1 results in specific radiosensitization of HPV-positive HNSCC cells.MATERIALS AND METHODS: Experiments were performed with five HPV and p16-positive (93-VU-147T, UM-SCC-47, UT-SCC-45, UD-SCC-2, UPCI-SCC-154) and two HPV and p16-negative HNSCC cell lines, as well as two normal human fibroblast strains. Chk1 was inhibited by the selective inhibitor PF-00477736. Cell cycle distribution was determined by flow cytometry, Chk1-activity via Western blot and cell survival by colony formation assay.RESULTS: With the exception of UPCI-SCC-154, the inhibition of Chk1 was found to abolish the pronounced radiation-induced G2-arrest in all HPV-positive cells utilized. All tumor cell lines that demonstrated the abrogation of G2-arrest also demonstrated radiosensitization. Notably, in G1-arrest-proficient normal human fibroblasts no radiosensitization was induced.CONCLUSION: Abrogation of the G2 checkpoint through the inhibition of Chk1 may be used to selectively increase the cellular radiosensitivity of HPV-positive HNSCC without affecting the surrounding normal tissue.",
author = "Chia-Jung Busch and Malte Kriegs and Simon Laban and Silke Tribius and Rainald Knecht and Cordula Petersen and Ekkehard Dikomey and Thorsten Rieckmann",
note = "Copyright {\textcopyright} 2013 Elsevier Ireland Ltd. All rights reserved.",
year = "2013",
month = sep,
day = "1",
doi = "10.1016/j.radonc.2013.06.035",
language = "English",
volume = "108",
pages = "495--9",
journal = "RADIOTHER ONCOL",
issn = "0167-8140",
publisher = "Elsevier Ireland Ltd",
number = "3",

}

RIS

TY - JOUR

T1 - HPV-positive HNSCC cell lines but not primary human fibroblasts are radiosensitized by the inhibition of Chk1

AU - Busch, Chia-Jung

AU - Kriegs, Malte

AU - Laban, Simon

AU - Tribius, Silke

AU - Knecht, Rainald

AU - Petersen, Cordula

AU - Dikomey, Ekkehard

AU - Rieckmann, Thorsten

N1 - Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.

PY - 2013/9/1

Y1 - 2013/9/1

N2 - PURPOSE: Despite the comparably high cure rates observed for HPV-positive HNSCC, there is still a great need for specific tumor radiosensitization due to the often severe side effects resulting from intense radiochemotherapy. We recently demonstrated that HPV-positive HNSCC cell lines are characterized by a defect in DNA double-strand break repair associated with a pronounced G2-arrest. Here we tested whether abrogation of this radiation-induced G2-arrest by the inhibition of Chk1 results in specific radiosensitization of HPV-positive HNSCC cells.MATERIALS AND METHODS: Experiments were performed with five HPV and p16-positive (93-VU-147T, UM-SCC-47, UT-SCC-45, UD-SCC-2, UPCI-SCC-154) and two HPV and p16-negative HNSCC cell lines, as well as two normal human fibroblast strains. Chk1 was inhibited by the selective inhibitor PF-00477736. Cell cycle distribution was determined by flow cytometry, Chk1-activity via Western blot and cell survival by colony formation assay.RESULTS: With the exception of UPCI-SCC-154, the inhibition of Chk1 was found to abolish the pronounced radiation-induced G2-arrest in all HPV-positive cells utilized. All tumor cell lines that demonstrated the abrogation of G2-arrest also demonstrated radiosensitization. Notably, in G1-arrest-proficient normal human fibroblasts no radiosensitization was induced.CONCLUSION: Abrogation of the G2 checkpoint through the inhibition of Chk1 may be used to selectively increase the cellular radiosensitivity of HPV-positive HNSCC without affecting the surrounding normal tissue.

AB - PURPOSE: Despite the comparably high cure rates observed for HPV-positive HNSCC, there is still a great need for specific tumor radiosensitization due to the often severe side effects resulting from intense radiochemotherapy. We recently demonstrated that HPV-positive HNSCC cell lines are characterized by a defect in DNA double-strand break repair associated with a pronounced G2-arrest. Here we tested whether abrogation of this radiation-induced G2-arrest by the inhibition of Chk1 results in specific radiosensitization of HPV-positive HNSCC cells.MATERIALS AND METHODS: Experiments were performed with five HPV and p16-positive (93-VU-147T, UM-SCC-47, UT-SCC-45, UD-SCC-2, UPCI-SCC-154) and two HPV and p16-negative HNSCC cell lines, as well as two normal human fibroblast strains. Chk1 was inhibited by the selective inhibitor PF-00477736. Cell cycle distribution was determined by flow cytometry, Chk1-activity via Western blot and cell survival by colony formation assay.RESULTS: With the exception of UPCI-SCC-154, the inhibition of Chk1 was found to abolish the pronounced radiation-induced G2-arrest in all HPV-positive cells utilized. All tumor cell lines that demonstrated the abrogation of G2-arrest also demonstrated radiosensitization. Notably, in G1-arrest-proficient normal human fibroblasts no radiosensitization was induced.CONCLUSION: Abrogation of the G2 checkpoint through the inhibition of Chk1 may be used to selectively increase the cellular radiosensitivity of HPV-positive HNSCC without affecting the surrounding normal tissue.

U2 - 10.1016/j.radonc.2013.06.035

DO - 10.1016/j.radonc.2013.06.035

M3 - SCORING: Journal article

C2 - 23932155

VL - 108

SP - 495

EP - 499

JO - RADIOTHER ONCOL

JF - RADIOTHER ONCOL

SN - 0167-8140

IS - 3

ER -