Targeting NUPR1-dependent stress granules formation to induce synthetic lethality in KrasG12D-driven tumors
We find that NUPR1, a stress-associated intrinsically disordered protein, induced droplet formation via liquid–liquid phase separation (LLPS). NUPR1-driven LLPS was crucial for the creation of NUPR1-dependent stress granules (SGs) in pancreatic cancer cells since genetic or pharmacological inhibitio...
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| Vydáno v: | EMBO molecular medicine Ročník 16; číslo 3; s. 475 - 505 |
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| Hlavní autoři: | , , , , , , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
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London
Nature Publishing Group UK
14.03.2024
Wiley Open Access Springer Nature |
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| ISSN: | 1757-4684, 1757-4676, 1757-4684 |
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| Abstract | We find that NUPR1, a stress-associated intrinsically disordered protein, induced droplet formation via liquid–liquid phase separation (LLPS). NUPR1-driven LLPS was crucial for the creation of NUPR1-dependent stress granules (SGs) in pancreatic cancer cells since genetic or pharmacological inhibition by ZZW-115 of NUPR1 activity impeded SGs formation. The Kras
G12D
mutation induced oncogenic stress, NUPR1 overexpression, and promoted SGs development. Notably, enforced NUPR1 expression induced SGs formation independently of mutated Kras
G12D
. Mechanistically, Kras
G12D
expression strengthened sensitivity to NUPR1 inactivation, inducing cell death, activating caspase 3 and releasing LDH. Remarkably, ZZW-115-mediated SG-formation inhibition hampered the development of pancreatic intraepithelial neoplasia (PanINs) in
Pdx1-cre;LSL-Kras
G12D
(KC) mice. ZZW-115-treatment of KC mice triggered caspase 3 activation, DNA fragmentation, and formation of the apoptotic bodies, leading to cell death, specifically in Kras
G12D
-expressing cells. We further demonstrated that, in developed PanINs, short-term ZZW-115 treatment prevented NUPR1-associated SGs presence. Lastly, a four-week ZZW-115 treatment significantly reduced the number and size of PanINs in KC mice. This study proposes that targeting NUPR1-dependent SGs formation could be a therapeutic approach to induce cell death in Kras
G12D
-dependent tumors.
Synopsis
Activation of kras oncogene induces, on one hand, a strong oncogenic stress, and on the other hand, a concomitant stress response, including the activation of the stress protein NUPR1, which in turn induces the formation of SGs through its ability to undergo LLPS.
Enforced NUPR1 expression induced SGs formation, independently of mutated KrasG12D, which played a protective role in the cell.
Inhibition of ZZW-115-mediated SGs-formation hampered the development of PanINs in Pdx1-cre;LSL-KrasG12D (KC) mice.
ZZW-115-treatment of KC mice triggered caspase 3 activation, DNA fragmentation, and formation of apoptotic bodies, leading to cell death, specifically in KrasG12D-expressing cells.
Targeting NUPR1-dependent SGs formation could be a therapeutic approach to induce cell death in KrasG12D-dependent tumors.
Activation of kras oncogene induces, on one hand, a strong oncogenic stress, and on the other hand, a concomitant stress response, including the activation of the stress protein NUPR1, which in turn induces the formation of SGs through its ability to undergo LLPS. |
|---|---|
| AbstractList | We find that NUPR1, a stress-associated intrinsically disordered protein, induced droplet formation via liquid-liquid phase separation (LLPS). NUPR1-driven LLPS was crucial for the creation of NUPR1-dependent stress granules (SGs) in pancreatic cancer cells since genetic or pharmacological inhibition by ZZW-115 of NUPR1 activity impeded SGs formation. The KrasG12D mutation induced oncogenic stress, NUPR1 overexpression, and promoted SGs development. Notably, enforced NUPR1 expression induced SGs formation independently of mutated KrasG12D. Mechanistically, KrasG12D expression strengthened sensitivity to NUPR1 inactivation, inducing cell death, activating caspase 3 and releasing LDH. Remarkably, ZZW-115-mediated SG-formation inhibition hampered the development of pancreatic intraepithelial neoplasia (PanINs) in Pdx1-cre;LSL-KrasG12D (KC) mice. ZZW-115-treatment of KC mice triggered caspase 3 activation, DNA fragmentation, and formation of the apoptotic bodies, leading to cell death, specifically in KrasG12D-expressing cells. We further demonstrated that, in developed PanINs, short-term ZZW-115 treatment prevented NUPR1-associated SGs presence. Lastly, a four-week ZZW-115 treatment significantly reduced the number and size of PanINs in KC mice. This study proposes that targeting NUPR1-dependent SGs formation could be a therapeutic approach to induce cell death in KrasG12D-dependent tumors.We find that NUPR1, a stress-associated intrinsically disordered protein, induced droplet formation via liquid-liquid phase separation (LLPS). NUPR1-driven LLPS was crucial for the creation of NUPR1-dependent stress granules (SGs) in pancreatic cancer cells since genetic or pharmacological inhibition by ZZW-115 of NUPR1 activity impeded SGs formation. The KrasG12D mutation induced oncogenic stress, NUPR1 overexpression, and promoted SGs development. Notably, enforced NUPR1 expression induced SGs formation independently of mutated KrasG12D. Mechanistically, KrasG12D expression strengthened sensitivity to NUPR1 inactivation, inducing cell death, activating caspase 3 and releasing LDH. Remarkably, ZZW-115-mediated SG-formation inhibition hampered the development of pancreatic intraepithelial neoplasia (PanINs) in Pdx1-cre;LSL-KrasG12D (KC) mice. ZZW-115-treatment of KC mice triggered caspase 3 activation, DNA fragmentation, and formation of the apoptotic bodies, leading to cell death, specifically in KrasG12D-expressing cells. We further demonstrated that, in developed PanINs, short-term ZZW-115 treatment prevented NUPR1-associated SGs presence. Lastly, a four-week ZZW-115 treatment significantly reduced the number and size of PanINs in KC mice. This study proposes that targeting NUPR1-dependent SGs formation could be a therapeutic approach to induce cell death in KrasG12D-dependent tumors. We find that NUPR1, a stress-associated intrinsically disordered protein, induced droplet formation via liquid–liquid phase separation (LLPS). NUPR1-driven LLPS was crucial for the creation of NUPR1-dependent stress granules (SGs) in pancreatic cancer cells since genetic or pharmacological inhibition by ZZW-115 of NUPR1 activity impeded SGs formation. The Kras G12D mutation induced oncogenic stress, NUPR1 overexpression, and promoted SGs development. Notably, enforced NUPR1 expression induced SGs formation independently of mutated Kras G12D . Mechanistically, Kras G12D expression strengthened sensitivity to NUPR1 inactivation, inducing cell death, activating caspase 3 and releasing LDH. Remarkably, ZZW-115-mediated SG-formation inhibition hampered the development of pancreatic intraepithelial neoplasia (PanINs) in Pdx1-cre;LSL-Kras G12D (KC) mice. ZZW-115-treatment of KC mice triggered caspase 3 activation, DNA fragmentation, and formation of the apoptotic bodies, leading to cell death, specifically in Kras G12D -expressing cells. We further demonstrated that, in developed PanINs, short-term ZZW-115 treatment prevented NUPR1-associated SGs presence. Lastly, a four-week ZZW-115 treatment significantly reduced the number and size of PanINs in KC mice. This study proposes that targeting NUPR1-dependent SGs formation could be a therapeutic approach to induce cell death in Kras G12D -dependent tumors. Abstract We find that NUPR1, a stress-associated intrinsically disordered protein, induced droplet formation via liquid–liquid phase separation (LLPS). NUPR1-driven LLPS was crucial for the creation of NUPR1-dependent stress granules (SGs) in pancreatic cancer cells since genetic or pharmacological inhibition by ZZW-115 of NUPR1 activity impeded SGs formation. The KrasG12D mutation induced oncogenic stress, NUPR1 overexpression, and promoted SGs development. Notably, enforced NUPR1 expression induced SGs formation independently of mutated KrasG12D. Mechanistically, KrasG12D expression strengthened sensitivity to NUPR1 inactivation, inducing cell death, activating caspase 3 and releasing LDH. Remarkably, ZZW-115-mediated SG-formation inhibition hampered the development of pancreatic intraepithelial neoplasia (PanINs) in Pdx1-cre;LSL-Kras G12D (KC) mice. ZZW-115-treatment of KC mice triggered caspase 3 activation, DNA fragmentation, and formation of the apoptotic bodies, leading to cell death, specifically in KrasG12D-expressing cells. We further demonstrated that, in developed PanINs, short-term ZZW-115 treatment prevented NUPR1-associated SGs presence. Lastly, a four-week ZZW-115 treatment significantly reduced the number and size of PanINs in KC mice. This study proposes that targeting NUPR1-dependent SGs formation could be a therapeutic approach to induce cell death in KrasG12D-dependent tumors. We find that NUPR1, a stress-associated intrinsically disordered protein, induced droplet formation via liquid–liquid phase separation (LLPS). NUPR1-driven LLPS was crucial for the creation of NUPR1-dependent stress granules (SGs) in pancreatic cancer cells since genetic or pharmacological inhibition by ZZW-115 of NUPR1 activity impeded SGs formation. The Kras G12D mutation induced oncogenic stress, NUPR1 overexpression, and promoted SGs development. Notably, enforced NUPR1 expression induced SGs formation independently of mutated Kras G12D . Mechanistically, Kras G12D expression strengthened sensitivity to NUPR1 inactivation, inducing cell death, activating caspase 3 and releasing LDH. Remarkably, ZZW-115-mediated SG-formation inhibition hampered the development of pancreatic intraepithelial neoplasia (PanINs) in Pdx1-cre;LSL-Kras G12D (KC) mice. ZZW-115-treatment of KC mice triggered caspase 3 activation, DNA fragmentation, and formation of the apoptotic bodies, leading to cell death, specifically in Kras G12D -expressing cells. We further demonstrated that, in developed PanINs, short-term ZZW-115 treatment prevented NUPR1-associated SGs presence. Lastly, a four-week ZZW-115 treatment significantly reduced the number and size of PanINs in KC mice. This study proposes that targeting NUPR1-dependent SGs formation could be a therapeutic approach to induce cell death in Kras G12D -dependent tumors. Synopsis Activation of kras oncogene induces, on one hand, a strong oncogenic stress, and on the other hand, a concomitant stress response, including the activation of the stress protein NUPR1, which in turn induces the formation of SGs through its ability to undergo LLPS. Enforced NUPR1 expression induced SGs formation, independently of mutated KrasG12D, which played a protective role in the cell. Inhibition of ZZW-115-mediated SGs-formation hampered the development of PanINs in Pdx1-cre;LSL-KrasG12D (KC) mice. ZZW-115-treatment of KC mice triggered caspase 3 activation, DNA fragmentation, and formation of apoptotic bodies, leading to cell death, specifically in KrasG12D-expressing cells. Targeting NUPR1-dependent SGs formation could be a therapeutic approach to induce cell death in KrasG12D-dependent tumors. Activation of kras oncogene induces, on one hand, a strong oncogenic stress, and on the other hand, a concomitant stress response, including the activation of the stress protein NUPR1, which in turn induces the formation of SGs through its ability to undergo LLPS. Abstract We find that NUPR1, a stress-associated intrinsically disordered protein, induced droplet formation via liquid–liquid phase separation (LLPS). NUPR1-driven LLPS was crucial for the creation of NUPR1-dependent stress granules (SGs) in pancreatic cancer cells since genetic or pharmacological inhibition by ZZW-115 of NUPR1 activity impeded SGs formation. The Kras G12D mutation induced oncogenic stress, NUPR1 overexpression, and promoted SGs development. Notably, enforced NUPR1 expression induced SGs formation independently of mutated Kras G12D . Mechanistically, Kras G12D expression strengthened sensitivity to NUPR1 inactivation, inducing cell death, activating caspase 3 and releasing LDH. Remarkably, ZZW-115-mediated SG-formation inhibition hampered the development of pancreatic intraepithelial neoplasia (PanINs) in Pdx1-cre;LSL-Kras G12D (KC) mice. ZZW-115-treatment of KC mice triggered caspase 3 activation, DNA fragmentation, and formation of the apoptotic bodies, leading to cell death, specifically in Kras G12D -expressing cells. We further demonstrated that, in developed PanINs, short-term ZZW-115 treatment prevented NUPR1-associated SGs presence. Lastly, a four-week ZZW-115 treatment significantly reduced the number and size of PanINs in KC mice. This study proposes that targeting NUPR1-dependent SGs formation could be a therapeutic approach to induce cell death in Kras G12D -dependent tumors. |
| Author | Bessone, Ivan Fernandez Soubeyran, Philippe Brenière, Manon Santofimia-Castaño, Patricia Audebert, Stephane Neira, Jose Luis di Magliano, Marina Pasca Camoin, Luc Estaras, Matias Fraunhoffer, Nicolas Liu, Xi Lomberk, Gwen Urrutia, Raul Modesti, Mauro Iovanna, Juan |
| Author_xml | – sequence: 1 givenname: Patricia orcidid: 0000-0003-2506-5567 surname: Santofimia-Castaño fullname: Santofimia-Castaño, Patricia email: patricia.santofimia@inserm.fr organization: Centre de Recherche en Cancérologie de Marseille (CRCM), INSERM U1068, CNRS UMR 7258, Aix-Marseille Université and Institut Paoli-Calmettes, Parc Scientifique et Technologique de Luminy – sequence: 2 givenname: Nicolas surname: Fraunhoffer fullname: Fraunhoffer, Nicolas organization: Centre de Recherche en Cancérologie de Marseille (CRCM), INSERM U1068, CNRS UMR 7258, Aix-Marseille Université and Institut Paoli-Calmettes, Parc Scientifique et Technologique de Luminy, Universidad de Buenos Aires, Consejo Nacional de investigaciones Científicas y Técnicas, Centro de Estudios Farmacológicos y Botánicos (CEFYBO), Facultad de Medicina – sequence: 3 givenname: Xi surname: Liu fullname: Liu, Xi organization: Centre de Recherche en Cancérologie de Marseille (CRCM), INSERM U1068, CNRS UMR 7258, Aix-Marseille Université and Institut Paoli-Calmettes, Parc Scientifique et Technologique de Luminy – sequence: 4 givenname: Ivan Fernandez surname: Bessone fullname: Bessone, Ivan Fernandez organization: Centre de Recherche en Cancérologie de Marseille (CRCM), INSERM U1068, CNRS UMR 7258, Aix-Marseille Université and Institut Paoli-Calmettes, Parc Scientifique et Technologique de Luminy – sequence: 5 givenname: Marina Pasca surname: di Magliano fullname: di Magliano, Marina Pasca organization: Department of Surgery, University of Michigan – sequence: 6 givenname: Stephane orcidid: 0000-0002-9409-2588 surname: Audebert fullname: Audebert, Stephane organization: Centre de Recherche en Cancérologie de Marseille (CRCM), INSERM U1068, CNRS UMR 7258, Aix-Marseille Université and Institut Paoli-Calmettes, Parc Scientifique et Technologique de Luminy – sequence: 7 givenname: Luc orcidid: 0000-0002-1230-4787 surname: Camoin fullname: Camoin, Luc organization: Centre de Recherche en Cancérologie de Marseille (CRCM), INSERM U1068, CNRS UMR 7258, Aix-Marseille Université and Institut Paoli-Calmettes, Parc Scientifique et Technologique de Luminy – sequence: 8 givenname: Matias surname: Estaras fullname: Estaras, Matias organization: Centre de Recherche en Cancérologie de Marseille (CRCM), INSERM U1068, CNRS UMR 7258, Aix-Marseille Université and Institut Paoli-Calmettes, Parc Scientifique et Technologique de Luminy – sequence: 9 givenname: Manon surname: Brenière fullname: Brenière, Manon organization: Centre de Recherche en Cancérologie de Marseille (CRCM), INSERM U1068, CNRS UMR 7258, Aix-Marseille Université and Institut Paoli-Calmettes, Parc Scientifique et Technologique de Luminy – sequence: 10 givenname: Mauro orcidid: 0000-0002-4964-331X surname: Modesti fullname: Modesti, Mauro organization: Centre de Recherche en Cancérologie de Marseille (CRCM), INSERM U1068, CNRS UMR 7258, Aix-Marseille Université and Institut Paoli-Calmettes, Parc Scientifique et Technologique de Luminy – sequence: 11 givenname: Gwen orcidid: 0000-0001-5463-789X surname: Lomberk fullname: Lomberk, Gwen organization: Division of Research, Department of Surgery, Medical College of Wisconsin – sequence: 12 givenname: Raul surname: Urrutia fullname: Urrutia, Raul organization: Genomic Science and Precision Medicine Center (GSPMC), Medical College of Wisconsin – sequence: 13 givenname: Philippe orcidid: 0000-0002-5876-3217 surname: Soubeyran fullname: Soubeyran, Philippe organization: Centre de Recherche en Cancérologie de Marseille (CRCM), INSERM U1068, CNRS UMR 7258, Aix-Marseille Université and Institut Paoli-Calmettes, Parc Scientifique et Technologique de Luminy – sequence: 14 givenname: Jose Luis orcidid: 0000-0002-4933-0428 surname: Neira fullname: Neira, Jose Luis organization: IDIBE, Universidad Miguel Hernández, Edificio Torregaitán, Avda. del Ferrocarril s/n, Instituto de Biocomputación y Física de Sistemas Complejos (BIFI), Universidad de Zaragoza – sequence: 15 givenname: Juan orcidid: 0000-0003-1822-2237 surname: Iovanna fullname: Iovanna, Juan email: juan.iovanna@inserm.fr organization: Centre de Recherche en Cancérologie de Marseille (CRCM), INSERM U1068, CNRS UMR 7258, Aix-Marseille Université and Institut Paoli-Calmettes, Parc Scientifique et Technologique de Luminy, Equipe Labellisée La Ligue, Hospital de Alta Complejidad El Cruce, Florencio Varela, University Arturo Jauretche, Florencio Varela |
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| Snippet | We find that NUPR1, a stress-associated intrinsically disordered protein, induced droplet formation via liquid–liquid phase separation (LLPS). NUPR1-driven... We find that NUPR1, a stress-associated intrinsically disordered protein, induced droplet formation via liquid-liquid phase separation (LLPS). NUPR1-driven... Abstract We find that NUPR1, a stress-associated intrinsically disordered protein, induced droplet formation via liquid–liquid phase separation (LLPS).... |
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| SubjectTerms | Biomedical and Life Sciences Biomedicine EMBO03 EMBO12 Kras Life Sciences Molecular Medicine NUPR1 Stress Granules Synthetic Lethality ZZW-115 |
| Title | Targeting NUPR1-dependent stress granules formation to induce synthetic lethality in KrasG12D-driven tumors |
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