A novel small molecule Enpp1 inhibitor improves tumor control following radiation therapy by targeting stromal Enpp1 expression

Abstract The uniqueness in each person’s cancer cells and variation in immune infiltrates means that each tumor represents a unique problem, but therapeutic targets can be found among their shared features. Radiation therapy alters the interaction between the cancer cells and the stroma through rele...

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Main Authors: Jason R Baird, Alejandro F Alice, Roland Saito, Qingqing Chai, Minhua Han, Cindy Ng, Stephanie Han, Beth Fernandez, Sarah Ledoux, Johannes Grosse, Alan J Korman, Megan Potuznik, Venkatesh Rajamanickam, Brady Bernard, Marka R Crittenden, Michael J Gough
Format: Article
Language:English
Published: Nature Portfolio 2024-12-01
Series:Scientific Reports
Online Access:https://doi.org/10.1038/s41598-024-80677-8
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author Jason R Baird
Alejandro F Alice
Roland Saito
Qingqing Chai
Minhua Han
Cindy Ng
Stephanie Han
Beth Fernandez
Sarah Ledoux
Johannes Grosse
Alan J Korman
Megan Potuznik
Venkatesh Rajamanickam
Brady Bernard
Marka R Crittenden
Michael J Gough
author_facet Jason R Baird
Alejandro F Alice
Roland Saito
Qingqing Chai
Minhua Han
Cindy Ng
Stephanie Han
Beth Fernandez
Sarah Ledoux
Johannes Grosse
Alan J Korman
Megan Potuznik
Venkatesh Rajamanickam
Brady Bernard
Marka R Crittenden
Michael J Gough
author_sort Jason R Baird
collection DOAJ
description Abstract The uniqueness in each person’s cancer cells and variation in immune infiltrates means that each tumor represents a unique problem, but therapeutic targets can be found among their shared features. Radiation therapy alters the interaction between the cancer cells and the stroma through release of innate adjuvants. The extranuclear DNA that can result from radiation damage of cells can result in production of the second messenger cyclic guanosine monophosphate–adenosine monophosphate (cGAMP) by cyclic GMP-AMP synthase (cGAS). In turn, cGAMP can activate the innate sensor stimulator of interferon genes (STING), resulting in innate immune activation. Ectonucleotide pyrophosphatase/phosphodiesterase 1 (Enpp1) is a phosphodiesterase that can be expressed by cancer cells that can degrade cGAMP, thus can decrease or block STING activation following radiation therapy, impairing the innate immunity that is critical to support adaptive immune control of tumors. We observed that many human and murine cancer cells lack Enpp1 expression, but that Enpp1 is expressed in cells of the tumor stroma where it limits tumor control by radiation therapy. We demonstrate in preclinical models the efficacy of a novel Enpp1 inhibitor and show that this inhibitor improves tumor control by radiation even where the cancer cells lack Enpp1. This mechanism requires STING and type I interferon (IFN) receptor expression by non-cancer cells and is dependent on CD8 T cells as a final effector mechanism of tumor control. This suggests that Enpp1 inhibition may be an effective partner for radiation therapy regardless of whether cancer cells express Enpp1. This broadens the potential patient base for whom Enpp1 inhibitors can be applied to improve innate immune responses following radiation therapy.
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spelling doaj-art-cbaeda0ee181438bbb8d05f9ec45b6602025-08-20T02:20:45ZengNature PortfolioScientific Reports2045-23222024-12-0114111710.1038/s41598-024-80677-8A novel small molecule Enpp1 inhibitor improves tumor control following radiation therapy by targeting stromal Enpp1 expressionJason R Baird0Alejandro F Alice1Roland Saito2Qingqing Chai3Minhua Han4Cindy Ng5Stephanie Han6Beth Fernandez7Sarah Ledoux8Johannes Grosse9Alan J Korman10Megan Potuznik11Venkatesh Rajamanickam12Brady Bernard13Marka R Crittenden14Michael J Gough15Earle A. Chiles Research Institute, Robert W. Franz Cancer Center, Providence Portland Medical CenterEarle A. Chiles Research Institute, Robert W. Franz Cancer Center, Providence Portland Medical CenterVIR Biotechnology IncVIR Biotechnology IncVIR Biotechnology IncVIR Biotechnology IncVIR Biotechnology IncVIR Biotechnology IncVIR Biotechnology IncVIR Biotechnology IncVIR Biotechnology IncEarle A. Chiles Research Institute, Robert W. Franz Cancer Center, Providence Portland Medical CenterEarle A. Chiles Research Institute, Robert W. Franz Cancer Center, Providence Portland Medical CenterEarle A. Chiles Research Institute, Robert W. Franz Cancer Center, Providence Portland Medical CenterEarle A. Chiles Research Institute, Robert W. Franz Cancer Center, Providence Portland Medical CenterEarle A. Chiles Research Institute, Robert W. Franz Cancer Center, Providence Portland Medical CenterAbstract The uniqueness in each person’s cancer cells and variation in immune infiltrates means that each tumor represents a unique problem, but therapeutic targets can be found among their shared features. Radiation therapy alters the interaction between the cancer cells and the stroma through release of innate adjuvants. The extranuclear DNA that can result from radiation damage of cells can result in production of the second messenger cyclic guanosine monophosphate–adenosine monophosphate (cGAMP) by cyclic GMP-AMP synthase (cGAS). In turn, cGAMP can activate the innate sensor stimulator of interferon genes (STING), resulting in innate immune activation. Ectonucleotide pyrophosphatase/phosphodiesterase 1 (Enpp1) is a phosphodiesterase that can be expressed by cancer cells that can degrade cGAMP, thus can decrease or block STING activation following radiation therapy, impairing the innate immunity that is critical to support adaptive immune control of tumors. We observed that many human and murine cancer cells lack Enpp1 expression, but that Enpp1 is expressed in cells of the tumor stroma where it limits tumor control by radiation therapy. We demonstrate in preclinical models the efficacy of a novel Enpp1 inhibitor and show that this inhibitor improves tumor control by radiation even where the cancer cells lack Enpp1. This mechanism requires STING and type I interferon (IFN) receptor expression by non-cancer cells and is dependent on CD8 T cells as a final effector mechanism of tumor control. This suggests that Enpp1 inhibition may be an effective partner for radiation therapy regardless of whether cancer cells express Enpp1. This broadens the potential patient base for whom Enpp1 inhibitors can be applied to improve innate immune responses following radiation therapy.https://doi.org/10.1038/s41598-024-80677-8
spellingShingle Jason R Baird
Alejandro F Alice
Roland Saito
Qingqing Chai
Minhua Han
Cindy Ng
Stephanie Han
Beth Fernandez
Sarah Ledoux
Johannes Grosse
Alan J Korman
Megan Potuznik
Venkatesh Rajamanickam
Brady Bernard
Marka R Crittenden
Michael J Gough
A novel small molecule Enpp1 inhibitor improves tumor control following radiation therapy by targeting stromal Enpp1 expression
Scientific Reports
title A novel small molecule Enpp1 inhibitor improves tumor control following radiation therapy by targeting stromal Enpp1 expression
title_full A novel small molecule Enpp1 inhibitor improves tumor control following radiation therapy by targeting stromal Enpp1 expression
title_fullStr A novel small molecule Enpp1 inhibitor improves tumor control following radiation therapy by targeting stromal Enpp1 expression
title_full_unstemmed A novel small molecule Enpp1 inhibitor improves tumor control following radiation therapy by targeting stromal Enpp1 expression
title_short A novel small molecule Enpp1 inhibitor improves tumor control following radiation therapy by targeting stromal Enpp1 expression
title_sort novel small molecule enpp1 inhibitor improves tumor control following radiation therapy by targeting stromal enpp1 expression
url https://doi.org/10.1038/s41598-024-80677-8
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