Chromosomal instability triggers cell death via local signalling through the innate immune receptor Toll

Dawei Liu; Zeeshan Shaukat; Robert Saint; Stephen Gregory

doi:10.18632/oncotarget.6035

Chromosomal instability triggers cell death via local signalling through the innate immune receptor Toll

Dawei Liu, Zeeshan Shaukat, Robert Saint, Stephen Gregory

Deputy Vice-Chancellor (Research)

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Abstract

Chromosomal instability (CIN) is a hallmark of cancer and has been implicated in cancer initiation, progression and the development of resistance to traditional cancer therapy. Here we identify a new property of CIN cells, showing that inducing CIN in proliferating Drosophila larval tissue leads to the activation of innate immune signalling in CIN cells. Manipulation of this immune pathway strongly affects the survival of CIN cells, primarily via JNK, which responds to both Toll and TNFα/Eiger. This pathway also activates Mmp1, which recruits hemocytes to the CIN tissue to provide local amplification of the immune response that is needed for effective elimination of CIN cells.

Original language	English
Pages (from-to)	38552-38565
Number of pages	14
Journal	Oncotarget
Volume	6
Issue number	36
DOIs	https://doi.org/10.18632/oncotarget.6035
Publication status	Published - 8 Oct 2015

Bibliographical note

All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.

Keywords

chromosomal instability
innate immune response
Drosophila
TNFα
TLRs
Immunology Section
immunity
immune response

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abstract = "Chromosomal instability (CIN) is a hallmark of cancer and has been implicated in cancer initiation, progression and the development of resistance to traditional cancer therapy. Here we identify a new property of CIN cells, showing that inducing CIN in proliferating Drosophila larval tissue leads to the activation of innate immune signalling in CIN cells. Manipulation of this immune pathway strongly affects the survival of CIN cells, primarily via JNK, which responds to both Toll and TNFα/Eiger. This pathway also activates Mmp1, which recruits hemocytes to the CIN tissue to provide local amplification of the immune response that is needed for effective elimination of CIN cells.",

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AU - Liu, Dawei

AU - Shaukat, Zeeshan

AU - Saint, Robert

AU - Gregory, Stephen

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N2 - Chromosomal instability (CIN) is a hallmark of cancer and has been implicated in cancer initiation, progression and the development of resistance to traditional cancer therapy. Here we identify a new property of CIN cells, showing that inducing CIN in proliferating Drosophila larval tissue leads to the activation of innate immune signalling in CIN cells. Manipulation of this immune pathway strongly affects the survival of CIN cells, primarily via JNK, which responds to both Toll and TNFα/Eiger. This pathway also activates Mmp1, which recruits hemocytes to the CIN tissue to provide local amplification of the immune response that is needed for effective elimination of CIN cells.

AB - Chromosomal instability (CIN) is a hallmark of cancer and has been implicated in cancer initiation, progression and the development of resistance to traditional cancer therapy. Here we identify a new property of CIN cells, showing that inducing CIN in proliferating Drosophila larval tissue leads to the activation of innate immune signalling in CIN cells. Manipulation of this immune pathway strongly affects the survival of CIN cells, primarily via JNK, which responds to both Toll and TNFα/Eiger. This pathway also activates Mmp1, which recruits hemocytes to the CIN tissue to provide local amplification of the immune response that is needed for effective elimination of CIN cells.

KW - chromosomal instability

KW - innate immune response

KW - Drosophila

KW - TNFα

KW - TLRs

KW - Immunology Section

KW - immunity

KW - immune response

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JF - Oncotarget

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Chromosomal instability triggers cell death via local signalling through the innate immune receptor Toll

Abstract

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