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PARP Inhibitors and Proteins Interacting with SLX4

SIMPLE SUMMARY: The aim of this review is to highlight recent work performed on the activity of a class of cancer drugs (PARP inhibitor) in various cell lines, either expressing or not expressing proteins interacting with the DNA repair protein SLX4. This could be at the basis of the development of...

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Autor principal: Jordheim, Lars Petter
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9913592/
https://www.ncbi.nlm.nih.gov/pubmed/36765954
http://dx.doi.org/10.3390/cancers15030997
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author Jordheim, Lars Petter
author_facet Jordheim, Lars Petter
author_sort Jordheim, Lars Petter
collection PubMed
description SIMPLE SUMMARY: The aim of this review is to highlight recent work performed on the activity of a class of cancer drugs (PARP inhibitor) in various cell lines, either expressing or not expressing proteins interacting with the DNA repair protein SLX4. This could be at the basis of the development of new therapeutic strategies in cancer treatment. ABSTRACT: PARP inhibitors are small molecules currently used with success in the treatment of certain cancer patients. Their action was first shown to be specific to cells with DNA repair deficiencies, such as BRCA-mutant cancers. However, recent work has suggested clinical interest of these drugs beyond this group of patients. Preclinical data on relationships between the activity of PARP inhibitors and other proteins involved in DNA repair exist, and this review will only highlight findings on the SLX4 protein and its interacting protein partners. As suggested from these available data and depending on further validations, new treatment strategies could be developed in order to broaden the use for PARP inhibitors in cancer patients.
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spelling pubmed-99135922023-02-11 PARP Inhibitors and Proteins Interacting with SLX4 Jordheim, Lars Petter Cancers (Basel) Review SIMPLE SUMMARY: The aim of this review is to highlight recent work performed on the activity of a class of cancer drugs (PARP inhibitor) in various cell lines, either expressing or not expressing proteins interacting with the DNA repair protein SLX4. This could be at the basis of the development of new therapeutic strategies in cancer treatment. ABSTRACT: PARP inhibitors are small molecules currently used with success in the treatment of certain cancer patients. Their action was first shown to be specific to cells with DNA repair deficiencies, such as BRCA-mutant cancers. However, recent work has suggested clinical interest of these drugs beyond this group of patients. Preclinical data on relationships between the activity of PARP inhibitors and other proteins involved in DNA repair exist, and this review will only highlight findings on the SLX4 protein and its interacting protein partners. As suggested from these available data and depending on further validations, new treatment strategies could be developed in order to broaden the use for PARP inhibitors in cancer patients. MDPI 2023-02-03 /pmc/articles/PMC9913592/ /pubmed/36765954 http://dx.doi.org/10.3390/cancers15030997 Text en © 2023 by the author. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Jordheim, Lars Petter
PARP Inhibitors and Proteins Interacting with SLX4
title PARP Inhibitors and Proteins Interacting with SLX4
title_full PARP Inhibitors and Proteins Interacting with SLX4
title_fullStr PARP Inhibitors and Proteins Interacting with SLX4
title_full_unstemmed PARP Inhibitors and Proteins Interacting with SLX4
title_short PARP Inhibitors and Proteins Interacting with SLX4
title_sort parp inhibitors and proteins interacting with slx4
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9913592/
https://www.ncbi.nlm.nih.gov/pubmed/36765954
http://dx.doi.org/10.3390/cancers15030997
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