UCHL1 is a potential molecular indicator and therapeutic target for neuroendocrine carcinomas

Neuroendocrine carcinomas, such as neuroendocrine prostate cancer and small-cell lung cancer, commonly have a poor prognosis and limited therapeutic options. We report that ubiquitin carboxy-terminal hydrolase L1 (UCHL1), a deubiquitinating enzyme, is elevated in tissues and plasma from patients wit...

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Published inCell reports. Medicine Vol. 5; no. 2; p. 101381
Main Authors Liu, Shiqin, Chai, Timothy, Garcia-Marques, Fernando, Yin, Qingqing, Hsu, En-Chi, Shen, Michelle, Shaw Toland, Angus Martin, Bermudez, Abel, Hartono, Alifiani B., Massey, Christopher F., Lee, Chung S., Zheng, Liwei, Baron, Maya, Denning, Caden J., Aslan, Merve, Nguyen, Holly M., Nolley, Rosalie, Zoubeidi, Amina, Das, Millie, Kunder, Christian A., Howitt, Brooke E., Soh, H. Tom, Weissman, Irving L., Liss, Michael A., Chin, Arnold I., Brooks, James D., Corey, Eva, Pitteri, Sharon J., Huang, Jiaoti, Stoyanova, Tanya
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LanguageEnglish
Published United States Elsevier Inc 20.02.2024
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Abstract Neuroendocrine carcinomas, such as neuroendocrine prostate cancer and small-cell lung cancer, commonly have a poor prognosis and limited therapeutic options. We report that ubiquitin carboxy-terminal hydrolase L1 (UCHL1), a deubiquitinating enzyme, is elevated in tissues and plasma from patients with neuroendocrine carcinomas. Loss of UCHL1 decreases tumor growth and inhibits metastasis of these malignancies. UCHL1 maintains neuroendocrine differentiation and promotes cancer progression by regulating nucleoporin, POM121, and p53. UCHL1 binds, deubiquitinates, and stabilizes POM121 to regulate POM121-associated nuclear transport of E2F1 and c-MYC. Treatment with the UCHL1 inhibitor LDN-57444 slows tumor growth and metastasis across neuroendocrine carcinomas. The combination of UCHL1 inhibitors with cisplatin, the standard of care used for neuroendocrine carcinomas, significantly delays tumor growth in pre-clinical settings. Our study reveals mechanisms of UCHL1 function in regulating the progression of neuroendocrine carcinomas and identifies UCHL1 as a therapeutic target and potential molecular indicator for diagnosing and monitoring treatment responses in these malignancies. [Display omitted] •UCHL1 is a potential molecular indicator for neuroendocrine carcinomas•UCHL1 regulates neuroendocrine carcinoma tumor growth and metastasis•UCHL1 stabilizes POM121 and regulates POM121-driven E2F1 nuclear localization•UCHL1 is a therapeutic target for neuroendocrine carcinomas and neuroblastoma Liu et al. identify UCHL1 as a blood and tissue marker that is elevated across cancers with neuroendocrine features. These cancers are characterized by poor patient outcomes and lack effective treatments. UCHL1 inhibition exhibits anticancer effects in malignancies with neuroendocrine features, presenting a potent therapeutic strategy for these patients.
AbstractList Neuroendocrine carcinomas, such as neuroendocrine prostate cancer and small-cell lung cancer, commonly have a poor prognosis and limited therapeutic options. We report that ubiquitin carboxy-terminal hydrolase L1 (UCHL1), a deubiquitinating enzyme, is elevated in tissues and plasma from patients with neuroendocrine carcinomas. Loss of UCHL1 decreases tumor growth and inhibits metastasis of these malignancies. UCHL1 maintains neuroendocrine differentiation and promotes cancer progression by regulating nucleoporin, POM121, and p53. UCHL1 binds, deubiquitinates, and stabilizes POM121 to regulate POM121-associated nuclear transport of E2F1 and c-MYC. Treatment with the UCHL1 inhibitor LDN-57444 slows tumor growth and metastasis across neuroendocrine carcinomas. The combination of UCHL1 inhibitors with cisplatin, the standard of care used for neuroendocrine carcinomas, significantly delays tumor growth in pre-clinical settings. Our study reveals mechanisms of UCHL1 function in regulating the progression of neuroendocrine carcinomas and identifies UCHL1 as a therapeutic target and potential molecular indicator for diagnosing and monitoring treatment responses in these malignancies.
Neuroendocrine carcinomas, such as neuroendocrine prostate cancer and small-cell lung cancer, commonly have a poor prognosis and limited therapeutic options. We report that ubiquitin carboxy-terminal hydrolase L1 (UCHL1), a deubiquitinating enzyme, is elevated in tissues and plasma from patients with neuroendocrine carcinomas. Loss of UCHL1 decreases tumor growth and inhibits metastasis of these malignancies. UCHL1 maintains neuroendocrine differentiation and promotes cancer progression by regulating nucleoporin, POM121, and p53. UCHL1 binds, deubiquitinates, and stabilizes POM121 to regulate POM121-associated nuclear transport of E2F1 and c-MYC. Treatment with the UCHL1 inhibitor LDN-57444 slows tumor growth and metastasis across neuroendocrine carcinomas. The combination of UCHL1 inhibitors with cisplatin, the standard of care used for neuroendocrine carcinomas, significantly delays tumor growth in pre-clinical settings. Our study reveals mechanisms of UCHL1 function in regulating the progression of neuroendocrine carcinomas and identifies UCHL1 as a therapeutic target and potential molecular indicator for diagnosing and monitoring treatment responses in these malignancies. • UCHL1 is a potential molecular indicator for neuroendocrine carcinomas • UCHL1 regulates neuroendocrine carcinoma tumor growth and metastasis • UCHL1 stabilizes POM121 and regulates POM121-driven E2F1 nuclear localization • UCHL1 is a therapeutic target for neuroendocrine carcinomas and neuroblastoma Liu et al. identify UCHL1 as a blood and tissue marker that is elevated across cancers with neuroendocrine features. These cancers are characterized by poor patient outcomes and lack effective treatments. UCHL1 inhibition exhibits anticancer effects in malignancies with neuroendocrine features, presenting a potent therapeutic strategy for these patients.
Neuroendocrine carcinomas, such as neuroendocrine prostate cancer and small-cell lung cancer, commonly have a poor prognosis and limited therapeutic options. We report that ubiquitin carboxy-terminal hydrolase L1 (UCHL1), a deubiquitinating enzyme, is elevated in tissues and plasma from patients with neuroendocrine carcinomas. Loss of UCHL1 decreases tumor growth and inhibits metastasis of these malignancies. UCHL1 maintains neuroendocrine differentiation and promotes cancer progression by regulating nucleoporin, POM121, and p53. UCHL1 binds, deubiquitinates, and stabilizes POM121 to regulate POM121-associated nuclear transport of E2F1 and c-MYC. Treatment with the UCHL1 inhibitor LDN-57444 slows tumor growth and metastasis across neuroendocrine carcinomas. The combination of UCHL1 inhibitors with cisplatin, the standard of care used for neuroendocrine carcinomas, significantly delays tumor growth in pre-clinical settings. Our study reveals mechanisms of UCHL1 function in regulating the progression of neuroendocrine carcinomas and identifies UCHL1 as a therapeutic target and potential molecular indicator for diagnosing and monitoring treatment responses in these malignancies. [Display omitted] •UCHL1 is a potential molecular indicator for neuroendocrine carcinomas•UCHL1 regulates neuroendocrine carcinoma tumor growth and metastasis•UCHL1 stabilizes POM121 and regulates POM121-driven E2F1 nuclear localization•UCHL1 is a therapeutic target for neuroendocrine carcinomas and neuroblastoma Liu et al. identify UCHL1 as a blood and tissue marker that is elevated across cancers with neuroendocrine features. These cancers are characterized by poor patient outcomes and lack effective treatments. UCHL1 inhibition exhibits anticancer effects in malignancies with neuroendocrine features, presenting a potent therapeutic strategy for these patients.
ArticleNumber 101381
Author Liss, Michael A.
Huang, Jiaoti
Garcia-Marques, Fernando
Shaw Toland, Angus Martin
Massey, Christopher F.
Stoyanova, Tanya
Weissman, Irving L.
Baron, Maya
Chin, Arnold I.
Pitteri, Sharon J.
Aslan, Merve
Bermudez, Abel
Corey, Eva
Nolley, Rosalie
Hartono, Alifiani B.
Brooks, James D.
Howitt, Brooke E.
Nguyen, Holly M.
Soh, H. Tom
Kunder, Christian A.
Zoubeidi, Amina
Das, Millie
Yin, Qingqing
Hsu, En-Chi
Lee, Chung S.
Liu, Shiqin
Shen, Michelle
Zheng, Liwei
Chai, Timothy
Denning, Caden J.
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Issue 2
Keywords neuroblastoma
nuclear pore complex
UCHL1
small cell lung cancer
neuroendocrine carcinomas
neuroendocrine prostate cancer
Language English
License This is an open access article under the CC BY-NC-ND license.
Copyright © 2023 The Author(s). Published by Elsevier Inc. All rights reserved.
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Snippet Neuroendocrine carcinomas, such as neuroendocrine prostate cancer and small-cell lung cancer, commonly have a poor prognosis and limited therapeutic options....
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StartPage 101381
SubjectTerms Carcinoma, Neuroendocrine - drug therapy
Carcinoma, Neuroendocrine - genetics
Humans
Lung Neoplasms - diagnosis
Lung Neoplasms - drug therapy
Male
Membrane Glycoproteins
neuroblastoma
neuroendocrine carcinomas
neuroendocrine prostate cancer
nuclear pore complex
small cell lung cancer
Small Cell Lung Carcinoma
Ubiquitin Thiolesterase - genetics
Ubiquitin Thiolesterase - metabolism
UCHL1
Title UCHL1 is a potential molecular indicator and therapeutic target for neuroendocrine carcinomas
URI https://dx.doi.org/10.1016/j.xcrm.2023.101381
https://www.ncbi.nlm.nih.gov/pubmed/38244540
https://search.proquest.com/docview/2917863857
https://pubmed.ncbi.nlm.nih.gov/PMC10897521
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