Dataset Information

Protein paucimannosylation is a novel N-glycosylation signature of human cancers

ABSTRACT: While aberrant protein glycosylation is a recognised characteristic of human cancers, advances in glycoanalytics continue to discover new associations between glycoproteins and tumourigenesis. This glycomics-centric study investigates a possible link between protein paucimannosylation, an under-studied class of human N-glycosylation [Man1-3GlcNAc2Fuc0-1] and human cancers. The distribution of paucimannosidic glycans (PMGs) within the N-glycome of 34 cancer cell lines and 133 tissue samples spanning 11 prevalent cancer types and matching non-cancerous specimens were accurately determined from 467 PGC-LC-MS/MS datasets collected over a decade within our laboratories. PMGs, particularly the α1,6-fucosylated bi- and tri-mannosylated N-glycans, were prominent features of 29 cancer cell lines, but the PMG level varied dramatically across and within the investigated cancer types (1.0%-50.2%). Analyses of paired (tumour/non-tumour) and stage-stratified tissue cohorts demonstrated that PMGs are significantly enriched in tumours from four cancer types including liver and colorectal cancer and increase with prostate cancer and chronic lymphocytic leukaemia progression. Cancer cell surface expression of paucimannosidic proteins was demonstrated using immunofluorescence while biosynthetic involvement of β-hexosaminidase was indicated by quantitative proteomics. The intriguing association between protein paucimannosylation and human cancers reported here warrants further exploration to detail the biosynthesis, cellular location(s), protein carriers and functions of paucimannosylation in tumourigenesis and metastasis.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Prostate Adenocarcinoma Cell

DISEASE(S): Prostate Cancer

SUBMITTER: Rebeca Kawahara

LAB HEAD: Morten Thaysen-Andersen

PROVIDER: PXD014271 | Pride | 2021-03-07

REPOSITORIES: Pride

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Protein Paucimannosylation Is an Enriched N-Glycosylation Signature of Human Cancers.

Chatterjee Sayantani S Lee Ling Y LY Kawahara Rebeca R Abrahams Jodie L JL Adamczyk Barbara B Anugraham Merrina M Ashwood Christopher C Sumer-Bayraktar Zeynep Z Briggs Matthew T MT Chik Jenny H L JHL Everest-Dass Arun A Förster Sarah S Hinneburg Hannes H Leite Katia R M KRM Loke Ian I Möginger Uwe U Moh Edward S X ESX Nakano Miyako M Recuero Saulo S Sethi Manveen K MK Srougi Miguel M Stavenhagen Kathrin K Venkatakrishnan Vignesh V Wongtrakul-Kish Katherine K Diestel Simone S Hoffmann Peter P Karlsson Niclas G NG Kolarich Daniel D Molloy Mark P MP Muders Michael H MH Oehler Martin K MK Packer Nicolle H NH Palmisano Giuseppe G Thaysen-Andersen Morten M

Proteomics 20191016 21-22

While aberrant protein glycosylation is a recognized characteristic of human cancers, advances in glycoanalytics continue to discover new associations between glycoproteins and tumorigenesis. This glycomics-centric study investigates a possible link between protein paucimannosylation, an under-studied class of human N-glycosylation [Man1-3 GlcNAc2 Fuc0-1 ], and cancer. The paucimannosidic glycans (PMGs) of 34 cancer cell lines and 133 tissue samples spanning 11 c ...[more]

PMID: 31419058

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Project description:Tumor microenvironment coevolves with and simultaneously sustains cancer progression. Reactive fibroblasts found in prostate cancer (PCa), known as cancer associated fibroblasts (CAF), have been indeed shown to fuel tumor development and metastasis by mutually interacting with PCa cells. Little is known about the molecular mechanisms that lead to activation of CAFs from tissue-resident fibroblasts, circulating marrow-derived fibroblast progenitors or mesenchymal stem cells. Through integrated gene and microRNA expression profiling, here we showed that transcriptome of CAFs isolated from prostate tumors strictly resembles that of normal fibroblasts stimulated in vitro with interleukin-6 (IL6), thus confirming the capability of the cytokine to promote acquisition of an activated and cancer-promoting phenotype, and, for the first time, proving that IL6 is able per se to induce all the complex transcriptional changes characteristic of patient-derived CAFs. 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			Action	DRS
	HUMAN.fasta	Fasta
	RK_050519_TMTF1_1.raw	Raw
	RK_050519_TMTF1_2.raw	Raw
	RK_050519_TMTF1_3.raw	Raw
	RK_050519_TMTF2_1.raw	Raw