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Senescent cells communicate via intercellular protein transfer.

Abstract：

:Mammalian cells mostly rely on extracellular molecules to transfer signals to other cells. However, in stress conditions, more robust mechanisms might be necessary to facilitate cell-cell communications. Cellular senescence, a stress response associated with permanent exit from the cell cycle and the development of an immunogenic phenotype, limits both tumorigenesis and tissue damage. Paradoxically, the long-term presence of senescent cells can promote tissue damage and aging within their microenvironment. Soluble factors secreted from senescent cells mediate some of these cell-nonautonomous effects. However, it is unknown whether senescent cells impact neighboring cells by other mechanisms. Here we show that senescent cells directly transfer proteins to neighboring cells and that this process facilitates immune surveillance of senescent cells by natural killer (NK) cells. We found that transfer of proteins to NK and T cells is increased in the murine preneoplastic pancreas, a site where senescent cells are present in vivo. Proteomic analysis and functional studies of the transferred proteins revealed that the transfer is strictly dependent on cell-cell contact and CDC42-regulated actin polymerization and is mediated at least partially by cytoplasmic bridges. These findings reveal a novel mode of intercellular communication by which senescent cells regulate their immune surveillance and might impact tumorigenesis and tissue aging.

journal_name

Genes Dev

journal_title

Genes & development

authors

Biran A,Perelmutter M,Gal H,Burton DG,Ovadya Y,Vadai E,Geiger T,Krizhanovsky V

doi

10.1101/gad.259341.115

subject

Has Abstract

pub_date

2015-04-15 00:00:00

pages

791-802

issue

8

eissn

0890-9369

issn

1549-5477

pii

gad.259341.115

journal_volume

29

pub_type

杂志文章

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