Modelling stromal compartments to recapitulate the ameloblastoma tumour microenvironment.

3D models AM, Ameloblastoma BPE, Bovine pituitary extract BSA, Bovine serum albumin CCN, Cellular communication network factor 2 DMEM, Dulbecco’s modified Eagle medium ECM, Extracellular matrix FBS, Foetal bovine serum Fibroblasts H&E, Haematoxylin and eosin HFF-2, Human fibroblasts (HFF-2) HGF, Primary gingival fibroblasts IF, Immunofluorescence IHC IHC, Immunohistochemistry M, Molar MEM, Minimal Essential Medium MIQE, Minimum Information for Publication of Quantitative Real-Time PCR Experiments MMPs, Matrix metalloproteinases MRC5, Human lung fibroblasts Min, Minutes N.A, Neutralising agent PTHLH, Parathyroid Hormone Like Hormone RANK, The tumour necrosis factor (TNF) superfamily members receptor activator of nuclear factor kappa-B receptor RANKL RANKL, The tumour necrosis factor (TNF) superfamily members receptor activator of nuclear factor kappa-B ligand (TNFSF11) RT, Room temperature SD, Standard deviation SEM, Standard error mean SPARC, anti-osteonectin TGF-β, Transforming growth factor TME, Tumour microenvironment TNF, Tumour necrosis factor Tumour microenvironment dl-CGH, Double-layered collagen gel hemisphere hOB, Human osteoblasts α-SMA, alpha-smooth muscle actin

Journal

Matrix biology plus
ISSN: 2590-0285
Titre abrégé: Matrix Biol Plus
Pays: Netherlands
ID NLM: 101775320

Informations de publication

Date de publication:
Dec 2022
Historique:
received: 29 09 2022
revised: 03 11 2022
accepted: 18 11 2022
entrez: 1 12 2022
pubmed: 2 12 2022
medline: 2 12 2022
Statut: epublish

Résumé

Tumour development and progression is dependent upon tumour cell interaction with the tissue stroma. Bioengineering the tumour-stroma microenvironment (TME) into 3D biomimetic models is crucial to gain insight into tumour cell development and progression pathways and identify therapeutic targets. Ameloblastoma is a benign but locally aggressive epithelial odontogenic neoplasm that mainly occurs in the jawbone and can cause significant morbidity and sometimes death. The molecular mechanisms for ameloblastoma progression are poorly understood. A spatial model recapitulating the tumour and stroma was engineered to show that without a relevant stromal population, tumour invasion is quantitatively decreased. Where a relevant stroma was engineered in dense collagen populated by gingival fibroblasts, enhanced receptor activator of nuclear factor kappa-B ligand (RANKL) expression was observed and histopathological properties, including ameloblastoma tumour islands, developed and were quantified. Using human osteoblasts (bone stroma) further enhanced the biomimicry of ameloblastoma histopathological phenotypes. This work demonstrates the importance of the two key stromal populations, osteoblasts, and gingival fibroblasts, for accurate 3D biomimetic ameloblastoma modelling.

Identifiants

DOI: 10.1016/j.mbplus.2022.100125 PMID: 36452176 PMC: PMC9703037
pubmed: 36452176
doi: 10.1016/j.mbplus.2022.100125
pii: S2590-0285(22)00025-4
pmc: PMC9703037
doi:

Types de publication

Journal Article

Langues

eng

Pagination

100125

Informations de copyright

Crown Copyright © 2022 Published by Elsevier B.V.

Déclaration de conflit d'intérêts

The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

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Auteurs

Deniz Bakkalci (D)

UCL Centre for 3D Models of Health and Disease, Division of Surgery and Interventional Science, University College London, Charles Bell House, 43-45 Foley Street, W1W 7TS London, UK.

Amir Zaki Abdullah Zubir (AZA)

Unit of Oral and Maxillofacial Pathology, School of Clinical Dentistry, University of Sheffield, 19 Claremont Crescent, S10 2TA Sheffield, UK.

Syed Ali Khurram (SA)

Unit of Oral and Maxillofacial Pathology, School of Clinical Dentistry, University of Sheffield, 19 Claremont Crescent, S10 2TA Sheffield, UK.

Judith Pape (J)

UCL Centre for 3D Models of Health and Disease, Division of Surgery and Interventional Science, University College London, Charles Bell House, 43-45 Foley Street, W1W 7TS London, UK.

Kristiina Heikinheimo (K)

Department of Oral and Maxillofacial Surgery, Institute of Dentistry, University of Turku and Turku University Hospital, Turku, Finland.

Stefano Fedele (S)

Eastman Dental Institute, University College London, London, UK.

Umber Cheema (U)

UCL Centre for 3D Models of Health and Disease, Division of Surgery and Interventional Science, University College London, Charles Bell House, 43-45 Foley Street, W1W 7TS London, UK.

Classifications MeSH