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Title: Mechanism of tumor‐suppressive cell competition in flies
Authors: Kanda, Hiroshi  kyouindb  KAKEN_id  orcid https://orcid.org/0000-0002-7922-7309 (unconfirmed)
Igaki, Tatsushi  kyouindb  KAKEN_id
Author's alias: 菅田, 浩司
井垣, 達吏
Keywords: cell competition
Drosophila
tumor suppression
Issue Date: Oct-2020
Publisher: Wiley
Journal title: Cancer Science
Volume: 111
Issue: 10
Start page: 3409
End page: 3415
Abstract: Oncogenic mutations often trigger antitumor cellular response such as induction of apoptosis or cellular senescence. Studies in the last decade have identified the presence of the third guardian against mutation‐induced tumorigenesis, namely “cell competition.” Cell competition is a context‐dependent cell elimination whereby cells with higher fitness eliminate neighboring cells with lower fitness by inducing cell death. While oncogene‐induced apoptosis or oncogene‐induced senescence acts as a cell‐autonomous tumor suppressor, cell competition protects the tissue from tumorigenesis via cell‐cell communication. For instance, in Drosophila epithelium, oncogenic cells with cell polarity mutations overproliferate and develop into tumors on their own but are eliminated from the tissue when surrounded by wild‐type cells. Genetic studies in flies have unraveled that such tumor‐suppressive cell competition is regulated by at least three mechanisms: direct cell‐cell interaction between polarity‐deficient cells and wild‐type cells, secreted factors from epithelial cells, and systemic factors from distant organs. Molecular manipulation of tumor‐suppressive cell competition could provide a novel therapeutic strategy against human cancers.
Rights: © 2020 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association. This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.
URI: http://hdl.handle.net/2433/255383
DOI(Published Version): 10.1111/cas.14575
PubMed ID: 32677169
Related Link: http://onlinelibrary.wiley.com/wol1/doi/10.1111/cas.14575/fullpdf
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