UGDH promotes tumor-initiating cells and a fibroinflammatory tumor microenvironment in ovarian cancer.


Journal

Journal of experimental & clinical cancer research : CR
ISSN: 1756-9966
Titre abrégé: J Exp Clin Cancer Res
Pays: England
ID NLM: 8308647

Informations de publication

Date de publication:
19 Oct 2023
Historique:
received: 28 04 2023
accepted: 02 09 2023
medline: 23 10 2023
pubmed: 20 10 2023
entrez: 20 10 2023
Statut: epublish

Résumé

Epithelial ovarian cancer (EOC) is a global health burden, with the poorest five-year survival rate of the gynecological malignancies due to diagnosis at advanced stage and high recurrence rate. Recurrence in EOC is driven by the survival of chemoresistant, stem-like tumor-initiating cells (TICs) that are supported by a complex extracellular matrix and immunosuppressive microenvironment. To target TICs to prevent recurrence, we identified genes critical for TIC viability from a whole genome siRNA screen. A top hit was the cancer-associated, proteoglycan subunit synthesis enzyme UDP-glucose dehydrogenase (UGDH). Immunohistochemistry was used to characterize UGDH expression in histological and molecular subtypes of EOC. EOC cell lines were subtyped according to the molecular subtypes and the functional effects of modulating UGDH expression in vitro and in vivo in C1/Mesenchymal and C4/Differentiated subtype cell lines was examined. High UGDH expression was observed in high-grade serous ovarian cancers and a distinctive survival prognostic for UGDH expression was revealed when serous cancers were stratified by molecular subtype. High UGDH was associated with a poor prognosis in the C1/Mesenchymal subtype and low UGDH was associated with poor prognosis in the C4/Differentiated subtype. Knockdown of UGDH in the C1/mesenchymal molecular subtype reduced spheroid formation and viability and reduced the CD133 + /ALDH These data show that modulation of UGDH expression in ovarian cancer reveals distinct roles for UGDH in the C1/Mesenchymal and C4/Differentiated molecular subtypes of EOC, influencing the tumor microenvironmental composition. UGDH is a strong potential therapeutic target in TICs, for the treatment of EOC, particularly in patients with the mesenchymal molecular subtype.

Sections du résumé

BACKGROUND BACKGROUND
Epithelial ovarian cancer (EOC) is a global health burden, with the poorest five-year survival rate of the gynecological malignancies due to diagnosis at advanced stage and high recurrence rate. Recurrence in EOC is driven by the survival of chemoresistant, stem-like tumor-initiating cells (TICs) that are supported by a complex extracellular matrix and immunosuppressive microenvironment. To target TICs to prevent recurrence, we identified genes critical for TIC viability from a whole genome siRNA screen. A top hit was the cancer-associated, proteoglycan subunit synthesis enzyme UDP-glucose dehydrogenase (UGDH).
METHODS METHODS
Immunohistochemistry was used to characterize UGDH expression in histological and molecular subtypes of EOC. EOC cell lines were subtyped according to the molecular subtypes and the functional effects of modulating UGDH expression in vitro and in vivo in C1/Mesenchymal and C4/Differentiated subtype cell lines was examined.
RESULTS RESULTS
High UGDH expression was observed in high-grade serous ovarian cancers and a distinctive survival prognostic for UGDH expression was revealed when serous cancers were stratified by molecular subtype. High UGDH was associated with a poor prognosis in the C1/Mesenchymal subtype and low UGDH was associated with poor prognosis in the C4/Differentiated subtype. Knockdown of UGDH in the C1/mesenchymal molecular subtype reduced spheroid formation and viability and reduced the CD133 + /ALDH
CONCLUSIONS CONCLUSIONS
These data show that modulation of UGDH expression in ovarian cancer reveals distinct roles for UGDH in the C1/Mesenchymal and C4/Differentiated molecular subtypes of EOC, influencing the tumor microenvironmental composition. UGDH is a strong potential therapeutic target in TICs, for the treatment of EOC, particularly in patients with the mesenchymal molecular subtype.

Identifiants

pubmed: 37858159
doi: 10.1186/s13046-023-02820-z
pii: 10.1186/s13046-023-02820-z
pmc: PMC10585874
doi:

Substances chimiques

RNA, Small Interfering 0
UGDH protein, human EC 1.1.1.22
Uridine Diphosphate Glucose Dehydrogenase EC 1.1.1.22

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

270

Subventions

Organisme : NIH HHS
ID : HHSN261200800001E
Pays : United States
Organisme : NCI NIH HHS
ID : ZIA BC011054
Pays : United States
Organisme : NCI NIH HHS
ID : HHSN261201800001C
Pays : United States
Organisme : Intramural NIH HHS
ID : ZIA BC011054
Pays : United States
Organisme : NIH HHS
ID : HHSN261201800001I
Pays : United States

Informations de copyright

© 2023. Italian National Cancer Institute ‘Regina Elena’.

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Auteurs

Brittney S Harrington (BS)

Women's Malignancies Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892, USA.

Rahul Kamdar (R)

Women's Malignancies Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892, USA.

Franklin Ning (F)

Women's Malignancies Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892, USA.

Soumya Korrapati (S)

Women's Malignancies Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892, USA.

Michael W Caminear (MW)

Women's Malignancies Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892, USA.

Lidia F Hernandez (LF)

Women's Malignancies Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892, USA.

Donna Butcher (D)

Molecular Histopathology Laboratory, Frederick National Laboratory for Cancer Research, NCI, Frederick, MD, 21702, USA.

Elijah F Edmondson (EF)

Molecular Histopathology Laboratory, Frederick National Laboratory for Cancer Research, NCI, Frederick, MD, 21702, USA.

Nadia Traficante (N)

Peter MacCallum Cancer Centre, Melbourne, VIC, Australia.
Sir Peter MacCallum Department of Oncology, The University of Melbourne, Melbourne, VIC, Australia.

Joy Hendley (J)

Peter MacCallum Cancer Centre, Melbourne, VIC, Australia.
Sir Peter MacCallum Department of Oncology, The University of Melbourne, Melbourne, VIC, Australia.

Madeline Gough (M)

Mater Brisbane Hospital, Mater Health Services, South Brisbane, QLD, 4101, Australia.
Mater Research Institute, The University of Queensland, Translational Research Institute, Woolloongabba, QLD, 4102, Australia.

Rebecca Rogers (R)

Mater Brisbane Hospital, Mater Health Services, South Brisbane, QLD, 4101, Australia.

Rohan Lourie (R)

Mater Brisbane Hospital, Mater Health Services, South Brisbane, QLD, 4101, Australia.
Mater Research Institute, The University of Queensland, Translational Research Institute, Woolloongabba, QLD, 4102, Australia.

Jyoti Shetty (J)

CCR Sequencing Facility, Leidos Biomedical Research, Inc., Frederick National Laboratory for Cancer Research, Frederick, MD, 21701, USA.

Bao Tran (B)

CCR Sequencing Facility, Leidos Biomedical Research, Inc., Frederick National Laboratory for Cancer Research, Frederick, MD, 21701, USA.

Fathi Elloumi (F)

Collaborative Bioinformatics Resource (CCBR), Center for Cancer Research (CCR), National Cancer Institute (NCI), National Institutes of Health, Bethesda, MD, USA.
Advanced Biomedical Computational Science, Frederick National Laboratory for Cancer Research, Frederick, MD, USA.

Abdalla Abdelmaksoud (A)

Collaborative Bioinformatics Resource (CCBR), Center for Cancer Research (CCR), National Cancer Institute (NCI), National Institutes of Health, Bethesda, MD, USA.
Advanced Biomedical Computational Science, Frederick National Laboratory for Cancer Research, Frederick, MD, USA.

Madhu Lal Nag (ML)

Collaborative Bioinformatics Resource (CCBR), Center for Cancer Research (CCR), National Cancer Institute (NCI), National Institutes of Health, Bethesda, MD, USA.
Advanced Biomedical Computational Science, Frederick National Laboratory for Cancer Research, Frederick, MD, USA.

Krystyna Mazan-Mamczarz (K)

Functional Genomics Lab, National Center for Advancing Translational Sciences, National Institutes of Health, Bethesda, MD, 20892, USA.

Carrie D House (CD)

Women's Malignancies Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892, USA.
Present address: Department of Biology, San Diego State University, San Diego, CA, 92182, USA.

John D Hooper (JD)

Mater Research Institute, The University of Queensland, Translational Research Institute, Woolloongabba, QLD, 4102, Australia.

Christina M Annunziata (CM)

Women's Malignancies Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892, USA. christina.annunziata@cancer.org.

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