TOPK modulates tumour-specific radiosensitivity and correlates with recurrence after prostate radiotherapy
Background: Tumour-specific radiosensitising treatments may enhance the efficacy of radiotherapy without exacerbating side effects. In this study we determined the radiation response following depletion or inhibition of TOPK, a mitogen-activated protein kinase kinase family Ser/Thr protein kinase th...
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| Published in: | British journal of cancer Vol. 117; no. 4; pp. 503 - 512 |
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| Main Authors: | , , , , , , , , , , , , |
| Format: | Journal Article |
| Language: | English |
| Published: |
London
Nature Publishing Group UK
08.08.2017
Nature Publishing Group |
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| ISSN: | 0007-0920, 1532-1827, 1532-1827 |
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| Abstract | Background:
Tumour-specific radiosensitising treatments may enhance the efficacy of radiotherapy without exacerbating side effects. In this study we determined the radiation response following depletion or inhibition of TOPK, a mitogen-activated protein kinase kinase family Ser/Thr protein kinase that is upregulated in many cancers.
Methods:
Radiation response was studied in a wide range of cancer cell lines and normal cells using colony formation assays. The effect on cell cycle progression was assessed and the relationship between TOPK expression and therapeutic efficacy was studied in a cohort of 128 prostate cancer patients treated with radical radiotherapy.
Results:
TOPK
knockdown did not alter radiation response in normal tissues, but significantly enhanced radiosensitivity in cancer cells. This result was recapitulated in TOPK knockout cells and with the TOPK inhibitor, OTS964. TOPK depletion altered the G
1
/S transition and G
2
/M arrest in response to radiation. Furthermore, TOPK depletion increased chromosomal aberrations, multinucleation and apoptotic cell death after irradiation. These results suggest a possible role for TOPK in the radiation-induced DNA damage checkpoints. These findings have clinical relevance, as elevated TOPK protein expression was associated with poorer clinical outcomes in prostate cancer patients treated with radical radiotherapy.
Conclusions:
This study demonstrates that TOPK disruption may cause tumour-specific radiosensitisation in multiple different tumour types. |
|---|---|
| AbstractList | Tumour-specific radiosensitising treatments may enhance the efficacy of radiotherapy without exacerbating side effects. In this study we determined the radiation response following depletion or inhibition of TOPK, a mitogen-activated protein kinase kinase family Ser/Thr protein kinase that is upregulated in many cancers.BACKGROUNDTumour-specific radiosensitising treatments may enhance the efficacy of radiotherapy without exacerbating side effects. In this study we determined the radiation response following depletion or inhibition of TOPK, a mitogen-activated protein kinase kinase family Ser/Thr protein kinase that is upregulated in many cancers.Radiation response was studied in a wide range of cancer cell lines and normal cells using colony formation assays. The effect on cell cycle progression was assessed and the relationship between TOPK expression and therapeutic efficacy was studied in a cohort of 128 prostate cancer patients treated with radical radiotherapy.METHODSRadiation response was studied in a wide range of cancer cell lines and normal cells using colony formation assays. The effect on cell cycle progression was assessed and the relationship between TOPK expression and therapeutic efficacy was studied in a cohort of 128 prostate cancer patients treated with radical radiotherapy.TOPK knockdown did not alter radiation response in normal tissues, but significantly enhanced radiosensitivity in cancer cells. This result was recapitulated in TOPK knockout cells and with the TOPK inhibitor, OTS964. TOPK depletion altered the G1/S transition and G2/M arrest in response to radiation. Furthermore, TOPK depletion increased chromosomal aberrations, multinucleation and apoptotic cell death after irradiation. These results suggest a possible role for TOPK in the radiation-induced DNA damage checkpoints. These findings have clinical relevance, as elevated TOPK protein expression was associated with poorer clinical outcomes in prostate cancer patients treated with radical radiotherapy.RESULTSTOPK knockdown did not alter radiation response in normal tissues, but significantly enhanced radiosensitivity in cancer cells. This result was recapitulated in TOPK knockout cells and with the TOPK inhibitor, OTS964. TOPK depletion altered the G1/S transition and G2/M arrest in response to radiation. Furthermore, TOPK depletion increased chromosomal aberrations, multinucleation and apoptotic cell death after irradiation. These results suggest a possible role for TOPK in the radiation-induced DNA damage checkpoints. These findings have clinical relevance, as elevated TOPK protein expression was associated with poorer clinical outcomes in prostate cancer patients treated with radical radiotherapy.This study demonstrates that TOPK disruption may cause tumour-specific radiosensitisation in multiple different tumour types.CONCLUSIONSThis study demonstrates that TOPK disruption may cause tumour-specific radiosensitisation in multiple different tumour types. Background: Tumour-specific radiosensitising treatments may enhance the efficacy of radiotherapy without exacerbating side effects. In this study we determined the radiation response following depletion or inhibition of TOPK, a mitogen-activated protein kinase kinase family Ser/Thr protein kinase that is upregulated in many cancers. Methods: Radiation response was studied in a wide range of cancer cell lines and normal cells using colony formation assays. The effect on cell cycle progression was assessed and the relationship between TOPK expression and therapeutic efficacy was studied in a cohort of 128 prostate cancer patients treated with radical radiotherapy. Results: TOPK knockdown did not alter radiation response in normal tissues, but significantly enhanced radiosensitivity in cancer cells. This result was recapitulated in TOPK knockout cells and with the TOPK inhibitor, OTS964. TOPK depletion altered the G 1 /S transition and G 2 /M arrest in response to radiation. Furthermore, TOPK depletion increased chromosomal aberrations, multinucleation and apoptotic cell death after irradiation. These results suggest a possible role for TOPK in the radiation-induced DNA damage checkpoints. These findings have clinical relevance, as elevated TOPK protein expression was associated with poorer clinical outcomes in prostate cancer patients treated with radical radiotherapy. Conclusions: This study demonstrates that TOPK disruption may cause tumour-specific radiosensitisation in multiple different tumour types. Background:Tumour-specific radiosensitising treatments may enhance the efficacy of radiotherapy without exacerbating side effects. In this study we determined the radiation response following depletion or inhibition of TOPK, a mitogen-activated protein kinase kinase family Ser/Thr protein kinase that is upregulated in many cancers.Methods:Radiation response was studied in a wide range of cancer cell lines and normal cells using colony formation assays. The effect on cell cycle progression was assessed and the relationship between TOPK expression and therapeutic efficacy was studied in a cohort of 128 prostate cancer patients treated with radical radiotherapy.Results:TOPK knockdown did not alter radiation response in normal tissues, but significantly enhanced radiosensitivity in cancer cells. This result was recapitulated in TOPK knockout cells and with the TOPK inhibitor, OTS964. TOPK depletion altered the G1 /S transition and G2 /M arrest in response to radiation. Furthermore, TOPK depletion increased chromosomal aberrations, multinucleation and apoptotic cell death after irradiation. These results suggest a possible role for TOPK in the radiation-induced DNA damage checkpoints. These findings have clinical relevance, as elevated TOPK protein expression was associated with poorer clinical outcomes in prostate cancer patients treated with radical radiotherapy.Conclusions:This study demonstrates that TOPK disruption may cause tumour-specific radiosensitisation in multiple different tumour types. Tumour-specific radiosensitising treatments may enhance the efficacy of radiotherapy without exacerbating side effects. In this study we determined the radiation response following depletion or inhibition of TOPK, a mitogen-activated protein kinase kinase family Ser/Thr protein kinase that is upregulated in many cancers. Radiation response was studied in a wide range of cancer cell lines and normal cells using colony formation assays. The effect on cell cycle progression was assessed and the relationship between TOPK expression and therapeutic efficacy was studied in a cohort of 128 prostate cancer patients treated with radical radiotherapy. TOPK knockdown did not alter radiation response in normal tissues, but significantly enhanced radiosensitivity in cancer cells. This result was recapitulated in TOPK knockout cells and with the TOPK inhibitor, OTS964. TOPK depletion altered the G /S transition and G /M arrest in response to radiation. Furthermore, TOPK depletion increased chromosomal aberrations, multinucleation and apoptotic cell death after irradiation. These results suggest a possible role for TOPK in the radiation-induced DNA damage checkpoints. These findings have clinical relevance, as elevated TOPK protein expression was associated with poorer clinical outcomes in prostate cancer patients treated with radical radiotherapy. This study demonstrates that TOPK disruption may cause tumour-specific radiosensitisation in multiple different tumour types. |
| Author | Higgins, Geoff S Harrap, Iona McKenna, William G Pirovano, Giacomo Herbert, Katharine J Verrill, Clare L Ashton, Thomas M Prevo, Remko Ryan, Anderson J Bryant, Richard J Cerundolo, Lucia Macaulay, Valentine Buffa, Francesca M |
| Author_xml | – sequence: 1 givenname: Giacomo surname: Pirovano fullname: Pirovano, Giacomo organization: CRUK/MRC Oxford Institute for Radiation Oncology, University of Oxford – sequence: 2 givenname: Thomas M surname: Ashton fullname: Ashton, Thomas M organization: CRUK/MRC Oxford Institute for Radiation Oncology, University of Oxford – sequence: 3 givenname: Katharine J surname: Herbert fullname: Herbert, Katharine J organization: CRUK/MRC Oxford Institute for Radiation Oncology, University of Oxford – sequence: 4 givenname: Richard J surname: Bryant fullname: Bryant, Richard J organization: CRUK/MRC Oxford Institute for Radiation Oncology, University of Oxford, Nuffield Department of Surgical Sciences, Oxford Cancer Research Centre, University of Oxford – sequence: 5 givenname: Clare L surname: Verrill fullname: Verrill, Clare L organization: Nuffield Department of Surgical Sciences, Oxford Cancer Research Centre, University of Oxford – sequence: 6 givenname: Lucia surname: Cerundolo fullname: Cerundolo, Lucia organization: Nuffield Department of Surgical Sciences, Oxford Cancer Research Centre, University of Oxford – sequence: 7 givenname: Francesca M surname: Buffa fullname: Buffa, Francesca M organization: CRUK/MRC Oxford Institute for Radiation Oncology, University of Oxford – sequence: 8 givenname: Remko surname: Prevo fullname: Prevo, Remko organization: CRUK/MRC Oxford Institute for Radiation Oncology, University of Oxford – sequence: 9 givenname: Iona surname: Harrap fullname: Harrap, Iona organization: CRUK/MRC Oxford Institute for Radiation Oncology, University of Oxford – sequence: 10 givenname: Anderson J surname: Ryan fullname: Ryan, Anderson J organization: CRUK/MRC Oxford Institute for Radiation Oncology, University of Oxford – sequence: 11 givenname: Valentine surname: Macaulay fullname: Macaulay, Valentine organization: CRUK/MRC Oxford Institute for Radiation Oncology, University of Oxford – sequence: 12 givenname: William G surname: McKenna fullname: McKenna, William G organization: CRUK/MRC Oxford Institute for Radiation Oncology, University of Oxford – sequence: 13 givenname: Geoff S surname: Higgins fullname: Higgins, Geoff S email: geoffrey.higgins@oncology.ox.ac.uk organization: CRUK/MRC Oxford Institute for Radiation Oncology, University of Oxford |
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10.1158/0008-5472.CAN-06-1601 – volume: 370 start-page: 231 year: 2007 end-page: 245 ident: CR2 article-title: A mitotic kinase TOPK enhances Cdk1/cyclin B1-dependent phosphorylation of PRC1 and promotes cytokinesis publication-title: J Mol Biol doi: 10.1016/j.jmb.2007.04.067 – volume: 136 start-page: 473 year: 2009 end-page: 484 ident: CR30 article-title: Aurora B-mediated abscission checkpoint protects against tetraploidization publication-title: Cell doi: 10.1016/j.cell.2008.12.020 – volume: 61 start-page: 7660 year: 2001 end-page: 7668 ident: CR3 article-title: Neither p21WAF1 nor 14-3-3sigma prevents G2 progression to mitotic catastrophe in human colon carcinoma cells after DNA damage, but p21WAF1 induces stable G1 arrest in resulting tetraploid cells publication-title: Cancer Res – volume: 102 start-page: 151 year: 2010 end-page: 161 ident: CR36 article-title: Prognostic and predictive value of TOPK stratified by KRAS and BRAF gene alterations in sporadic, hereditary and 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Tumour-specific radiosensitising treatments may enhance the efficacy of radiotherapy without exacerbating side effects. In this study we determined... Tumour-specific radiosensitising treatments may enhance the efficacy of radiotherapy without exacerbating side effects. In this study we determined the... Background:Tumour-specific radiosensitising treatments may enhance the efficacy of radiotherapy without exacerbating side effects. In this study we determined... |
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| SubjectTerms | 631/45/607/275 692/4028/67/589/466 692/699/67/1059/485 Apoptosis Apoptosis - drug effects Apoptosis - radiation effects Biomedical and Life Sciences Biomedicine Cancer Research Cell cycle Cell Cycle Checkpoints - drug effects Cell Cycle Checkpoints - genetics Cell Cycle Checkpoints - radiation effects Cell death Cell Line, Tumor Cell Nucleus - genetics Cell Nucleus - radiation effects Chromosome aberrations Chromosome Aberrations - drug effects Chromosome Aberrations - radiation effects DNA damage Drug Resistance Epidemiology Gene Knockdown Techniques HCT116 Cells HeLa Cells Humans Kinases Male MAP kinase Mitogen-Activated Protein Kinase Kinases - antagonists & inhibitors Mitogen-Activated Protein Kinase Kinases - genetics Mitogen-Activated Protein Kinase Kinases - metabolism Molecular Medicine Neoplasm Recurrence, Local - metabolism Oncology Prostate cancer Prostatic Neoplasms - metabolism Prostatic Neoplasms - radiotherapy Protein kinase Protein Kinase Inhibitors - pharmacology Proteins Quinolones - pharmacology Radiation therapy Radiation Tolerance - drug effects Radiation Tolerance - genetics Radiosensitivity Side effects Survival Rate Translational Therapeutics Tumor cell lines Tumors |
| Title | TOPK modulates tumour-specific radiosensitivity and correlates with recurrence after prostate radiotherapy |
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