Mechanisms and consequences of ATMIN repression in hypoxic conditions: roles for p53 and HIF-1
Hypoxia-induced replication stress is one of the most physiologically relevant signals known to activate ATM in tumors. Recently, the ATM interactor (ATMIN) was identified as critical for replication stress-induced activation of ATM in response to aphidicolin and hydroxyurea. This suggests an essent...
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| Vydáno v: | Scientific reports Ročník 6; číslo 1; s. 21698 |
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| Hlavní autoři: | , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
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Nature Publishing Group UK
15.02.2016
Nature Publishing Group |
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| ISSN: | 2045-2322, 2045-2322 |
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| Abstract | Hypoxia-induced replication stress is one of the most physiologically relevant signals known to activate ATM in tumors. Recently, the ATM interactor (ATMIN) was identified as critical for replication stress-induced activation of ATM in response to aphidicolin and hydroxyurea. This suggests an essential role for ATMIN in ATM regulation during hypoxia, which induces replication stress. However, ATMIN also has a role in base excision repair, a process that has been demonstrated to be repressed and less efficient in hypoxic conditions. Here, we demonstrate that ATMIN is dispensable for ATM activation in hypoxia and in contrast to ATM, does not affect cell survival and radiosensitivity in hypoxia. Instead, we show that in hypoxic conditions ATMIN expression is repressed. Repression of ATMIN in hypoxia is mediated by both p53 and HIF-1α in an oxygen dependent manner. The biological consequence of ATMIN repression in hypoxia is decreased expression of the target gene,
DYNLL1
. An expression signature associated with p53 activity was negatively correlated with DYNLL1 expression in patient samples further supporting the p53 dependent repression of DYNLL1. Together, these data demonstrate multiple mechanisms of ATMIN repression in hypoxia with consequences including impaired BER and down regulation of the ATMIN transcriptional target,
DYNLL1
. |
|---|---|
| AbstractList | Hypoxia-induced replication stress is one of the most physiologically relevant signals known to activate ATM in tumors. Recently, the ATM interactor (ATMIN) was identified as critical for replication stress-induced activation of ATM in response to aphidicolin and hydroxyurea. This suggests an essential role for ATMIN in ATM regulation during hypoxia, which induces replication stress. However, ATMIN also has a role in base excision repair, a process that has been demonstrated to be repressed and less efficient in hypoxic conditions. Here, we demonstrate that ATMIN is dispensable for ATM activation in hypoxia and in contrast to ATM, does not affect cell survival and radiosensitivity in hypoxia. Instead, we show that in hypoxic conditions ATMIN expression is repressed. Repression of ATMIN in hypoxia is mediated by both p53 and HIF-1α in an oxygen dependent manner. The biological consequence of ATMIN repression in hypoxia is decreased expression of the target gene, DYNLL1. An expression signature associated with p53 activity was negatively correlated with DYNLL1 expression in patient samples further supporting the p53 dependent repression of DYNLL1. Together, these data demonstrate multiple mechanisms of ATMIN repression in hypoxia with consequences including impaired BER and down regulation of the ATMIN transcriptional target, DYNLL1. Hypoxia-induced replication stress is one of the most physiologically relevant signals known to activate ATM in tumors. Recently, the ATM interactor (ATMIN) was identified as critical for replication stress-induced activation of ATM in response to aphidicolin and hydroxyurea. This suggests an essential role for ATMIN in ATM regulation during hypoxia, which induces replication stress. However, ATMIN also has a role in base excision repair, a process that has been demonstrated to be repressed and less efficient in hypoxic conditions. Here, we demonstrate that ATMIN is dispensable for ATM activation in hypoxia and in contrast to ATM, does not affect cell survival and radiosensitivity in hypoxia. Instead, we show that in hypoxic conditions ATMIN expression is repressed. Repression of ATMIN in hypoxia is mediated by both p53 and HIF-1α in an oxygen dependent manner. The biological consequence of ATMIN repression in hypoxia is decreased expression of the target gene, DYNLL1 . An expression signature associated with p53 activity was negatively correlated with DYNLL1 expression in patient samples further supporting the p53 dependent repression of DYNLL1. Together, these data demonstrate multiple mechanisms of ATMIN repression in hypoxia with consequences including impaired BER and down regulation of the ATMIN transcriptional target, DYNLL1 . |
| ArticleNumber | 21698 |
| Author | Bernhardt, Stephan Leszczynska, Katarzyna B. Biasoli, Deborah Giaccia, Amato J. Anbalagan, Selvakumar Hammond, Ester M. Göttgens, Eva-Leonne Olcina, Monica M. Ient, Jonathan |
| Author_xml | – sequence: 1 givenname: Katarzyna B. surname: Leszczynska fullname: Leszczynska, Katarzyna B. organization: Department of Oncology, Cancer Research UK and Medical Research Council Oxford Institute for Radiation Oncology, The University of Oxford – sequence: 2 givenname: Eva-Leonne surname: Göttgens fullname: Göttgens, Eva-Leonne organization: Department of Oncology, Cancer Research UK and Medical Research Council Oxford Institute for Radiation Oncology, The University of Oxford – sequence: 3 givenname: Deborah surname: Biasoli fullname: Biasoli, Deborah organization: Department of Oncology, Cancer Research UK and Medical Research Council Oxford Institute for Radiation Oncology, The University of Oxford – sequence: 4 givenname: Monica M. surname: Olcina fullname: Olcina, Monica M. organization: Division of Cancer and Radiation Oncology, Department of Radiation Oncology, Stanford University – sequence: 5 givenname: Jonathan surname: Ient fullname: Ient, Jonathan organization: Department of Oncology, Cancer Research UK and Medical Research Council Oxford Institute for Radiation Oncology, The University of Oxford – sequence: 6 givenname: Selvakumar surname: Anbalagan fullname: Anbalagan, Selvakumar organization: Department of Oncology, Cancer Research UK and Medical Research Council Oxford Institute for Radiation Oncology, The University of Oxford – sequence: 7 givenname: Stephan surname: Bernhardt fullname: Bernhardt, Stephan organization: Department of Oncology, Cancer Research UK and Medical Research Council Oxford Institute for Radiation Oncology, The University of Oxford – sequence: 8 givenname: Amato J. surname: Giaccia fullname: Giaccia, Amato J. organization: Division of Cancer and Radiation Oncology, Department of Radiation Oncology, Stanford University – sequence: 9 givenname: Ester M. surname: Hammond fullname: Hammond, Ester M. organization: Department of Oncology, Cancer Research UK and Medical Research Council Oxford Institute for Radiation Oncology, The University of Oxford |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/26875667$$D View this record in MEDLINE/PubMed |
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| CitedBy_id | crossref_primary_10_1016_j_ijrobp_2019_06_2531 crossref_primary_10_1084_jem_20220214 crossref_primary_10_1016_j_pharmthera_2019_07_002 crossref_primary_10_1093_mutage_gez019 crossref_primary_10_1038_s41467_017_02245_1 crossref_primary_10_1016_j_dnarep_2017_06_022 crossref_primary_10_3389_fcell_2021_626229 crossref_primary_10_1111_febs_14377 crossref_primary_10_1038_s41467_021_24066_z crossref_primary_10_1002_cbin_11352 crossref_primary_10_1016_j_molcel_2017_03_005 crossref_primary_10_1016_j_biopha_2017_09_026 crossref_primary_10_3389_fonc_2019_01563 crossref_primary_10_1016_j_radonc_2020_04_048 |
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| Title | Mechanisms and consequences of ATMIN repression in hypoxic conditions: roles for p53 and HIF-1 |
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