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Targeting SAMHD1: To overcome multiple anti-cancer drugs resistance in hematological malignancies

Sterile α motif and histidine/aspartic acid domain containing protein 1 (SAMHD1) is a deoxynucleoside triphosphate (dNTPs) triphosphohydrolase that can hydrolyze dNTPs into deoxynucleosides and triphosphates to keep the balance of the intracellular dNTPs pool. Moreover, it has been reported that SAM...

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Autores principales: Wang, Tao, Liu, Ping, Yang, Jianmin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Chongqing Medical University 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10308132/
https://www.ncbi.nlm.nih.gov/pubmed/37396510
http://dx.doi.org/10.1016/j.gendis.2022.06.001
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author Wang, Tao
Liu, Ping
Yang, Jianmin
author_facet Wang, Tao
Liu, Ping
Yang, Jianmin
author_sort Wang, Tao
collection PubMed
description Sterile α motif and histidine/aspartic acid domain containing protein 1 (SAMHD1) is a deoxynucleoside triphosphate (dNTPs) triphosphohydrolase that can hydrolyze dNTPs into deoxynucleosides and triphosphates to keep the balance of the intracellular dNTPs pool. Moreover, it has been reported that SAMHD1 plays a role in regulating cell proliferation and the cell cycle, maintaining genome stability and inhibiting innate immune responses. SAMHD1 activity is regulated by phosphorylation, oxidation, SUMOylation, and O-GlcNAcylation. SAMHD1 mutations have been reported to cause diseases, including chronic lymphocytic leukemia and mantle cell lymphoma. SAMHD1 expression in acute myeloid leukemia predicts inferior prognosis. Recently, it has been revealed that SAMHD1 mediates the resistance to anti-cancer drugs. This review will focus on SAMHD1 function and regulation, the association between SAMHD1 and hematological malignancies and will provide updated information on SAMHD1 mediating resistance to nucleoside analogue antimetabolites, topoisomerase inhibitors, platinum-derived agents and DNA hypomethylating agents. Furthermore, histone deacetylase inhibitors and tyrosine kinase inhibitors indirectly increase anti-cancer drug resistance by increasing SAMDH1 activity. We herein highlight the importance of the development of novel agents targeting SAMHD1 to overcome treatment resistance of hematological malignancies, which would be an opportunity to improve the outcome of patients with refractory hematological malignancies.
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spelling pubmed-103081322023-06-30 Targeting SAMHD1: To overcome multiple anti-cancer drugs resistance in hematological malignancies Wang, Tao Liu, Ping Yang, Jianmin Genes Dis Review Article Sterile α motif and histidine/aspartic acid domain containing protein 1 (SAMHD1) is a deoxynucleoside triphosphate (dNTPs) triphosphohydrolase that can hydrolyze dNTPs into deoxynucleosides and triphosphates to keep the balance of the intracellular dNTPs pool. Moreover, it has been reported that SAMHD1 plays a role in regulating cell proliferation and the cell cycle, maintaining genome stability and inhibiting innate immune responses. SAMHD1 activity is regulated by phosphorylation, oxidation, SUMOylation, and O-GlcNAcylation. SAMHD1 mutations have been reported to cause diseases, including chronic lymphocytic leukemia and mantle cell lymphoma. SAMHD1 expression in acute myeloid leukemia predicts inferior prognosis. Recently, it has been revealed that SAMHD1 mediates the resistance to anti-cancer drugs. This review will focus on SAMHD1 function and regulation, the association between SAMHD1 and hematological malignancies and will provide updated information on SAMHD1 mediating resistance to nucleoside analogue antimetabolites, topoisomerase inhibitors, platinum-derived agents and DNA hypomethylating agents. Furthermore, histone deacetylase inhibitors and tyrosine kinase inhibitors indirectly increase anti-cancer drug resistance by increasing SAMDH1 activity. We herein highlight the importance of the development of novel agents targeting SAMHD1 to overcome treatment resistance of hematological malignancies, which would be an opportunity to improve the outcome of patients with refractory hematological malignancies. Chongqing Medical University 2022-06-26 /pmc/articles/PMC10308132/ /pubmed/37396510 http://dx.doi.org/10.1016/j.gendis.2022.06.001 Text en © 2023 The Authors. Publishing services by Elsevier B.V. on behalf of KeAi Communications Co., Ltd. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
spellingShingle Review Article
Wang, Tao
Liu, Ping
Yang, Jianmin
Targeting SAMHD1: To overcome multiple anti-cancer drugs resistance in hematological malignancies
title Targeting SAMHD1: To overcome multiple anti-cancer drugs resistance in hematological malignancies
title_full Targeting SAMHD1: To overcome multiple anti-cancer drugs resistance in hematological malignancies
title_fullStr Targeting SAMHD1: To overcome multiple anti-cancer drugs resistance in hematological malignancies
title_full_unstemmed Targeting SAMHD1: To overcome multiple anti-cancer drugs resistance in hematological malignancies
title_short Targeting SAMHD1: To overcome multiple anti-cancer drugs resistance in hematological malignancies
title_sort targeting samhd1: to overcome multiple anti-cancer drugs resistance in hematological malignancies
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10308132/
https://www.ncbi.nlm.nih.gov/pubmed/37396510
http://dx.doi.org/10.1016/j.gendis.2022.06.001
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