增多的证据凸显细菌在促进肿瘤发生中所起的作用。其中的机制可能是多样的，且现在仍然不太清楚。在此，我们报道沙门氏菌感染导致宿主细胞蛋白质广泛的去乙酰化/乙酰化改变。哺乳动物细胞分裂周期42（CDC42）的乙酰化，在细菌感染后急剧下降，CDC42是Rho GTP酶家族的成员之一，参与了癌细胞中许多重要的信号通路。CDC42被SIRT2去乙酰化，被p300/CBP乙酰化。赖氨酸153处的非乙酰化CDC42显示其下游效应物PAK4的结合受损，p38和JNK的磷酸化受到抑制，从而导致细胞凋亡减少。K153乙酰化的减少还增强了结肠癌细胞的迁移和侵袭能力。结直肠癌患者的K153乙酰化水平降低，则预示着不良预后。综上所述，我们的发现表明，通过操纵CDC42的乙酰化调控CDC42-PAK轴，细菌感染诱导结直肠肿瘤发生的一种新机制。 版权所有：© 2023 Wang等人。这是一篇开放获取的文章，根据创作共用许可证，允许在任何媒介上自由使用、分发和复制，只要原作者和出处被标明。

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.Copyright: © 2023 Wang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.