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Cell-cell interactions that drive tumorigenesis in Drosophila

Cell-cell interactions within tumour microenvironment play crucial roles in tumorigenesis. Genetic mosaic techniques available in Drosophila have provided a powerful platform to study the basic principles of tumour growth and progression via cell-cell communications. This led to the identification o...

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Detalles Bibliográficos
Autores principales: Enomoto, Masato, Igaki, Tatsushi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9683056/
https://www.ncbi.nlm.nih.gov/pubmed/36413374
http://dx.doi.org/10.1080/19336934.2022.2148828
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author Enomoto, Masato
Igaki, Tatsushi
author_facet Enomoto, Masato
Igaki, Tatsushi
author_sort Enomoto, Masato
collection PubMed
description Cell-cell interactions within tumour microenvironment play crucial roles in tumorigenesis. Genetic mosaic techniques available in Drosophila have provided a powerful platform to study the basic principles of tumour growth and progression via cell-cell communications. This led to the identification of oncogenic cell-cell interactions triggered by endocytic dysregulation, mitochondrial dysfunction, cell polarity defects, or Src activation in Drosophila imaginal epithelia. Such oncogenic cooperations can be caused by interactions among epithelial cells, mesenchymal cells, and immune cells. Moreover, microenvironmental factors such as nutrients, local tissue structures, and endogenous growth signalling activities critically affect tumorigenesis. Dissecting various types of oncogenic cell-cell interactions at the single-cell level in Drosophila will greatly increase our understanding of how tumours progress in living animals.
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spelling pubmed-96830562022-11-24 Cell-cell interactions that drive tumorigenesis in Drosophila Enomoto, Masato Igaki, Tatsushi Fly (Austin) Review Cell-cell interactions within tumour microenvironment play crucial roles in tumorigenesis. Genetic mosaic techniques available in Drosophila have provided a powerful platform to study the basic principles of tumour growth and progression via cell-cell communications. This led to the identification of oncogenic cell-cell interactions triggered by endocytic dysregulation, mitochondrial dysfunction, cell polarity defects, or Src activation in Drosophila imaginal epithelia. Such oncogenic cooperations can be caused by interactions among epithelial cells, mesenchymal cells, and immune cells. Moreover, microenvironmental factors such as nutrients, local tissue structures, and endogenous growth signalling activities critically affect tumorigenesis. Dissecting various types of oncogenic cell-cell interactions at the single-cell level in Drosophila will greatly increase our understanding of how tumours progress in living animals. Taylor & Francis 2022-11-22 /pmc/articles/PMC9683056/ /pubmed/36413374 http://dx.doi.org/10.1080/19336934.2022.2148828 Text en © 2022 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. https://creativecommons.org/licenses/by/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review
Enomoto, Masato
Igaki, Tatsushi
Cell-cell interactions that drive tumorigenesis in Drosophila
title Cell-cell interactions that drive tumorigenesis in Drosophila
title_full Cell-cell interactions that drive tumorigenesis in Drosophila
title_fullStr Cell-cell interactions that drive tumorigenesis in Drosophila
title_full_unstemmed Cell-cell interactions that drive tumorigenesis in Drosophila
title_short Cell-cell interactions that drive tumorigenesis in Drosophila
title_sort cell-cell interactions that drive tumorigenesis in drosophila
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9683056/
https://www.ncbi.nlm.nih.gov/pubmed/36413374
http://dx.doi.org/10.1080/19336934.2022.2148828
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