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Glycobiology of Cancer
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Glycobiology of Cancer

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Macromolecules".

Deadline for manuscript submissions: closed (31 October 2020) | Viewed by 29215

Special Issue Editors

Dr. Rosa Peracaula

E-Mail
Guest Editor
Biochemistry and Molecular Biology Unit, Department of Biology, University of Girona, Girona, Spain
Interests: glycobiology; tumor markers; PSA; prostate cancer; pancreatic cancer; sialyltransferases
Dr. Jennifer Munkley

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Guest Editor
Newcastle University Biosciences Institute, International Centre for Life, Newcastle upon Tyne NE1 3BZ, UK
Interests: glycosylation; glycans; prostate cancer; glycosyltransferases; precision oncology; biomarkers
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Glycobiology is a subject with an important impact in several biomedical fields. In cancer, tumour cells show an altered pattern of their glycans, which influences the different steps of the tumour progression. The identification of some of the altered mechanisms that lead to the anomalous glycosylation in tumours has contributed to the development of potential cancer therapeutic targets. In addition, some of the altered glycoconjugates in cancer have shown their potential for improving cancer diagnostics. However, a major knowledge is required to understand the molecular basis that lead to these glycosylation changes in different tumour types as well as their specific involvement in tumour biology.

Contributions to this Special Issue will cover recent advances in identifying the underlying mechanisms of glycan alterations in different tumours as well as their influence in tumour development. In addition, the different contributions will provide new insights in the use of glycosylation alterations found in tumours to find novel cancer therapeutic strategies and to develop new diagnostics approaches.

Dr. Rosa Peracaula
Dr. Jennifer Munkley
Guest Editors

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Keywords

  • glycosylation
  • cancer
  • glycoproteins
  • glycolipids
  • glycosyltransferases
  • tumor makers

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Published Papers (6 papers)

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Research

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17 pages, 1365 KiB  
Article
Glycosylation in Indolent, Significant and Aggressive Prostate Cancer by Automated High-Throughput N-Glycan Profiling
by Sarah Gilgunn, Keefe Murphy, Henning Stöckmann, Paul J. Conroy, T. Brendan Murphy, R. William Watson, Richard J. O’Kennedy, Pauline M. Rudd and Radka Saldova
Int. J. Mol. Sci. 2020, 21(23), 9233; https://doi.org/10.3390/ijms21239233 - 3 Dec 2020
Cited by 15 | Viewed by 2874
Abstract
The diagnosis and treatment of prostate cancer (PCa) is a major health-care concern worldwide. This cancer can manifest itself in many distinct forms and the transition from clinically indolent PCa to the more invasive aggressive form remains poorly understood. It is now universally [...] Read more.
The diagnosis and treatment of prostate cancer (PCa) is a major health-care concern worldwide. This cancer can manifest itself in many distinct forms and the transition from clinically indolent PCa to the more invasive aggressive form remains poorly understood. It is now universally accepted that glycan expression patterns change with the cellular modifications that accompany the onset of tumorigenesis. The aim of this study was to investigate if differential glycosylation patterns could distinguish between indolent, significant, and aggressive PCa. Whole serum N-glycan profiling was carried out on 117 prostate cancer patients’ serum using our automated, high-throughput analysis platform for glycan-profiling which utilizes ultra-performance liquid chromatography (UPLC) to obtain high resolution separation of N-linked glycans released from the serum glycoproteins. We observed increases in hybrid, oligomannose, and biantennary digalactosylated monosialylated glycans (M5A1G1S1, M8, and A2G2S1), bisecting glycans (A2B, A2(6)BG1) and monoantennary glycans (A1), and decreases in triantennary trigalactosylated trisialylated glycans with and without core fucose (A3G3S3 and FA3G3S3) with PCa progression from indolent through significant and aggressive disease. These changes give us an insight into the disease pathogenesis and identify potential biomarkers for monitoring the PCa progression, however these need further confirmation studies. Full article
(This article belongs to the Special Issue Glycobiology of Cancer)
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16 pages, 3761 KiB  
Article
Role of NEU3 Overexpression in the Prediction of Efficacy of EGFR-Targeted Therapies in Colon Cancer Cell Lines
by Federica Bovio, Samantha Epistolio, Alessandra Mozzi, Eugenio Monti, Paola Fusi, Matilde Forcella and Milo Frattini
Int. J. Mol. Sci. 2020, 21(22), 8805; https://doi.org/10.3390/ijms21228805 - 20 Nov 2020
Cited by 9 | Viewed by 2766
Abstract
The epidermal growth factor receptor (EGFR), through the MAP kinase and PI3K-Akt-mTOR axis, plays a pivotal role in colorectal cancer (CRC) pathogenesis. The membrane-associated NEU3 sialidase interacts with and desialylates EGFR by promoting its dimerization and downstream effectors’ activation. Among the targeted therapies [...] Read more.
The epidermal growth factor receptor (EGFR), through the MAP kinase and PI3K-Akt-mTOR axis, plays a pivotal role in colorectal cancer (CRC) pathogenesis. The membrane-associated NEU3 sialidase interacts with and desialylates EGFR by promoting its dimerization and downstream effectors’ activation. Among the targeted therapies against EGFR, the monoclonal antibody cetuximab is active only in a subgroup of patients not carrying mutations in the MAP kinase pathway. In order to better understand the EGFR-NEU3 interplay and the mechanisms of pharmacological resistance, we investigated the role of NEU3 deregulation in cetuximab-treated CRC cell lines transiently transfected with NEU3 using Western blot analysis. Our results indicate that NEU3 overexpression can enhance EGFR activation only if EGFR is overexpressed, indicating the existence of a threshold for NEU3-mediated EGFR activation. This enhancement mainly leads to the constitutive activation of the MAP kinase pathway. Consequently, we suggest that the evaluation of NEU3 expression cannot entirely substitute the evaluation of EGFR because EGFR-negative cases cannot be stimulated by NEU3. Furthermore, NEU3-mediated hyperactivation of EGFR is counterbalanced by the administration of cetuximab, hypothesizing that a combined treatment of NEU3- and EGFR-targeted therapies may represent a valid option for CRC patients, which must be investigated in the future. Full article
(This article belongs to the Special Issue Glycobiology of Cancer)
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23 pages, 2837 KiB  
Article
L1CAM as an E-selectin Ligand in Colon Cancer
by Fanny M. Deschepper, Roberta Zoppi, Martina Pirro, Paul J. Hensbergen, Fabio Dall’Olio, Maximillianos Kotsias, Richard A. Gardner, Daniel I.R. Spencer and Paula A. Videira
Int. J. Mol. Sci. 2020, 21(21), 8286; https://doi.org/10.3390/ijms21218286 - 5 Nov 2020
Cited by 10 | Viewed by 4668
Abstract
Metastasis is the main cause of death among colorectal cancer (CRC) patients. E-selectin and its carbohydrate ligands, including sialyl Lewis X (sLeX) antigen, are key players in the binding of circulating tumor cells to the endothelium, which is one of the [...] Read more.
Metastasis is the main cause of death among colorectal cancer (CRC) patients. E-selectin and its carbohydrate ligands, including sialyl Lewis X (sLeX) antigen, are key players in the binding of circulating tumor cells to the endothelium, which is one of the major events leading to organ invasion. Nevertheless, the identity of the glycoprotein scaffolds presenting these glycans in CRC remains unclear. In this study, we firstly have characterized the glycoengineered cell line SW620 transfected with the fucosyltransferase 6 (FUT6) coding for the α1,3-fucosyltransferase 6 (FUT6), which is the main enzyme responsible for the synthesis of sLeX in CRC. The SW620FUT6 cell line expressed high levels of sLeX antigen and E-selectin ligands. Moreover, it displayed increased migration ability. E-selectin ligand glycoproteins were isolated from the SW620FUT6 cell line, identified by mass spectrometry, and validated by flow cytometry and Western blot (WB). The most prominent E-selectin ligand we identified was the neural cell adhesion molecule L1 (L1CAM). Previous studies have shown association of L1CAM with metastasis in cancer, thus the novel role as E-selectin counter-receptor contributes to understand the molecular mechanism involving L1CAM in metastasis formation. Full article
(This article belongs to the Special Issue Glycobiology of Cancer)
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19 pages, 3460 KiB  
Article
The Sda Synthase B4GALNT2 Reduces Malignancy and Stemness in Colon Cancer Cell Lines Independently of Sialyl Lewis X Inhibition
by Michela Pucci, Inês Gomes Ferreira, Nadia Malagolini, Manuela Ferracin and Fabio Dall’Olio
Int. J. Mol. Sci. 2020, 21(18), 6558; https://doi.org/10.3390/ijms21186558 - 8 Sep 2020
Cited by 13 | Viewed by 2924
Abstract
Background: The Sda antigen and its biosynthetic enzyme B4GALNT2 are highly expressed in healthy colon but undergo a variable down-regulation in colon cancer. The biosynthesis of the malignancy-associated sialyl Lewis x (sLex) antigen in normal and cancerous colon is mediated [...] Read more.
Background: The Sda antigen and its biosynthetic enzyme B4GALNT2 are highly expressed in healthy colon but undergo a variable down-regulation in colon cancer. The biosynthesis of the malignancy-associated sialyl Lewis x (sLex) antigen in normal and cancerous colon is mediated by fucosyltransferase 6 (FUT6) and is mutually exclusive from that of Sda. It is thought that the reduced malignancy associated with high B4GALNT2 was due to sLex inhibition. Methods: We transfected the cell lines SW480 and SW620, derived respectively from a primary tumor and a metastasis of the same patient, with the cDNAs of FUT6 or B4GALNT2, generating cell variants expressing either the sLex or the Sda antigens. Transfectants were analyzed for growth in poor adherence, wound healing, stemness and gene expression profile. Results: B4GALNT2/Sda expression down-regulated all malignancy-associated phenotypes in SW620 but only those associated with stemness in SW480. FUT6/sLex enhanced some malignancy-associated phenotypes in SW620, but had little effect in SW480. The impact on the transcriptome was stronger for FUT6 than for B4GALNT2 and only partially overlapping between SW480 and SW620. Conclusions: B4GALNT2/Sda inhibits the stemness-associated malignant phenotype, independently of sLex inhibition. The impact of glycosyltransferases on the phenotype and the transcriptome is highly cell-line specific. Full article
(This article belongs to the Special Issue Glycobiology of Cancer)
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24 pages, 5657 KiB  
Article
Knockdown of α2,3-Sialyltransferases Impairs Pancreatic Cancer Cell Migration, Invasion and E-selectin-Dependent Adhesion
by Pedro Enrique Guerrero, Laura Miró, Bin S. Wong, Anna Massaguer, Neus Martínez-Bosch, Rafael de Llorens, Pilar Navarro, Konstantinos Konstantopoulos, Esther Llop and Rosa Peracaula
Int. J. Mol. Sci. 2020, 21(17), 6239; https://doi.org/10.3390/ijms21176239 - 28 Aug 2020
Cited by 28 | Viewed by 4052
Abstract
Aberrant sialylation is frequently found in pancreatic ductal adenocarcinoma (PDA). α2,3-Sialyltransferases (α2,3-STs) ST3GAL3 and ST3GAL4 are overexpressed in PDA tissues and are responsible for increased biosynthesis of sialyl-Lewis (sLe) antigens, which play an important role in metastasis. This study addresses the effect of [...] Read more.
Aberrant sialylation is frequently found in pancreatic ductal adenocarcinoma (PDA). α2,3-Sialyltransferases (α2,3-STs) ST3GAL3 and ST3GAL4 are overexpressed in PDA tissues and are responsible for increased biosynthesis of sialyl-Lewis (sLe) antigens, which play an important role in metastasis. This study addresses the effect of α2,3-STs knockdown on the migratory and invasive phenotype of PDA cells, and on E-selectin-dependent adhesion. Characterization of the cell sialome, the α2,3-STs and fucosyltransferases involved in the biosynthesis of sLe antigens, using a panel of human PDA cells showed differences in the levels of sialylated determinants and α2,3-STs expression, reflecting their phenotypic heterogeneity. Knockdown of ST3GAL3 and ST3GAL4 in BxPC-3 and Capan-1 cells, which expressed moderate to high levels of sLe antigens and α2,3-STs, led to a significant reduction in sLex and in most cases in sLea, with slight increases in the α2,6-sialic acid content. Moreover, ST3GAL3 and ST3GAL4 downregulation resulted in a significant decrease in cell migration and invasion. Binding and rolling to E-selectin, which represent key steps in metastasis, were also markedly impaired in the α2,3-STs knockdown cells. Our results indicate that inhibition of ST3GAL3 and ST3GAL4 may be a novel strategy to block PDA metastasis, which is one of the reasons for its dismal prognosis. Full article
(This article belongs to the Special Issue Glycobiology of Cancer)
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Review

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22 pages, 5055 KiB  
Review
FUT8 Alpha-(1,6)-Fucosyltransferase in Cancer
by Kayla Bastian, Emma Scott, David J. Elliott and Jennifer Munkley
Int. J. Mol. Sci. 2021, 22(1), 455; https://doi.org/10.3390/ijms22010455 - 5 Jan 2021
Cited by 85 | Viewed by 10841
Abstract
Aberrant glycosylation is a universal feature of cancer cells that can impact all steps in tumour progression from malignant transformation to metastasis and immune evasion. One key change in tumour glycosylation is altered core fucosylation. Core fucosylation is driven by fucosyltransferase 8 (FUT8), [...] Read more.
Aberrant glycosylation is a universal feature of cancer cells that can impact all steps in tumour progression from malignant transformation to metastasis and immune evasion. One key change in tumour glycosylation is altered core fucosylation. Core fucosylation is driven by fucosyltransferase 8 (FUT8), which catalyses the addition of α1,6-fucose to the innermost GlcNAc residue of N-glycans. FUT8 is frequently upregulated in cancer, and plays a critical role in immune evasion, antibody-dependent cellular cytotoxicity (ADCC), and the regulation of TGF-β, EGF, α3β1 integrin and E-Cadherin. Here, we summarise the role of FUT8 in various cancers (including lung, liver, colorectal, ovarian, prostate, breast, melanoma, thyroid, and pancreatic), discuss the potential mechanisms involved, and outline opportunities to exploit FUT8 as a critical factor in cancer therapeutics in the future. Full article
(This article belongs to the Special Issue Glycobiology of Cancer)
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