N-Glycosylation Patterns Correlate with Hepatocellular Carcinoma Genetic Subtypes.
Journal
Molecular cancer research : MCR
ISSN: 1557-3125
Titre abrégé: Mol Cancer Res
Pays: United States
ID NLM: 101150042
Informations de publication
Date de publication:
11 2021
11 2021
Historique:
received:
21
05
2021
revised:
15
07
2021
accepted:
30
07
2021
pubmed:
13
8
2021
medline:
23
3
2022
entrez:
12
8
2021
Statut:
ppublish
Résumé
Hepatocellular carcinoma (HCC) is the second leading cause of cancer deaths globally, and the incidence rate in the United States is increasing. Studies have identified inter- and intratumor heterogeneity as histologic and/or molecular subtypes/variants associated with response to certain molecular targeted therapies. Spatial HCC tissue profiling of N-linked glycosylation by matrix-assisted laser desorption ionization imaging mass spectrometry (MALDI-IMS) may serve as a new method to evaluate the tumor heterogeneity. Previous work has identified significant changes in the N-linked glycosylation of HCC tumors but has not accounted for the heterogeneous genetic and molecular nature of HCC. To determine the correlation between HCC-specific N-glycosylation changes and genetic/molecular tumor features, we profiled HCC tissue samples with MALDI-IMS and correlated the spatial N-glycosylation with a widely used HCC molecular classification (Hoshida subtypes). MALDI-IMS data displayed trends that could approximately distinguish between subtypes, with subtype 1 demonstrating significantly dysregulated N-glycosylation versus adjacent nontumor tissue. Although there were no individual N-glycan structures that could identify specific subtypes, trends emerged regarding the correlation of branched glycan expression to HCC as a whole and fucosylated glycan expression to subtype 1 tumors specifically. IMPLICATIONS: Correlating N-glycosylation to specific subtypes offers the specific detection of subtypes of HCC, which could both enhance early HCC sensitivity and guide targeted clinical therapies.
Identifiants
pubmed: 34380744
pii: 1541-7786.MCR-21-0348
doi: 10.1158/1541-7786.MCR-21-0348
pmc: PMC8802325
mid: NIHMS1733800
doi:
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
1868-1877Subventions
Organisme : NIDDK NIH HHS
ID : P30 DK123704
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA233794
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA237659
Pays : United States
Organisme : NCI NIH HHS
ID : U01 CA226052
Pays : United States
Informations de copyright
©2021 American Association for Cancer Research.
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