In:
PLOS Pathogens, Public Library of Science (PLoS), Vol. 19, No. 2 ( 2023-2-22), p. e1011189-
Abstract:
Increasing evidence highlights the role of bacteria in promoting tumorigenesis. The underlying mechanisms may be diverse and remain poorly understood. Here, we report that Salmonella infection leads to extensive de/acetylation changes in host cell proteins. The acetylation of mammalian cell division cycle 42 (CDC42), a member of the Rho family of GTPases involved in many crucial signaling pathways in cancer cells, is drastically reduced after bacterial infection. CDC42 is deacetylated by SIRT2 and acetylated by p300/CBP. Non-acetylated CDC42 at lysine 153 shows an impaired binding of its downstream effector PAK4 and an attenuated phosphorylation of p38 and JNK, consequently reduces cell apoptosis. The reduction in K153 acetylation also enhances the migration and invasion ability of colon cancer cells. The low level of K153 acetylation in patients with colorectal cancer (CRC) predicts a poor prognosis. Taken together, our findings suggest a new mechanism of bacterial infection-induced promotion of colorectal tumorigenesis by modulation of the CDC42-PAK axis through manipulation of CDC42 acetylation.
Type of Medium:
Online Resource
ISSN:
1553-7374
DOI:
10.1371/journal.ppat.1011189
DOI:
10.1371/journal.ppat.1011189.g001
DOI:
10.1371/journal.ppat.1011189.g002
DOI:
10.1371/journal.ppat.1011189.g003
DOI:
10.1371/journal.ppat.1011189.g004
DOI:
10.1371/journal.ppat.1011189.g005
DOI:
10.1371/journal.ppat.1011189.g006
DOI:
10.1371/journal.ppat.1011189.g007
DOI:
10.1371/journal.ppat.1011189.g008
DOI:
10.1371/journal.ppat.1011189.s001
DOI:
10.1371/journal.ppat.1011189.s002
DOI:
10.1371/journal.ppat.1011189.s003
DOI:
10.1371/journal.ppat.1011189.s004
DOI:
10.1371/journal.ppat.1011189.s005
DOI:
10.1371/journal.ppat.1011189.s006
DOI:
10.1371/journal.ppat.1011189.s007
DOI:
10.1371/journal.ppat.1011189.s008
DOI:
10.1371/journal.ppat.1011189.s009
DOI:
10.1371/journal.ppat.1011189.s010
DOI:
10.1371/journal.ppat.1011189.s011
DOI:
10.1371/journal.ppat.1011189.s012
DOI:
10.1371/journal.ppat.1011189.r001
DOI:
10.1371/journal.ppat.1011189.r002
DOI:
10.1371/journal.ppat.1011189.r003
DOI:
10.1371/journal.ppat.1011189.r004
DOI:
10.1371/journal.ppat.1011189.r005
DOI:
10.1371/journal.ppat.1011189.r006
Language:
English
Publisher:
Public Library of Science (PLoS)
Publication Date:
2023
detail.hit.zdb_id:
2205412-1
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