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肠细菌蛋白 AvrA 促进结肠肿瘤发生,并激活结肠 β-连环蛋白信号通路。

Enteric bacterial protein AvrA promotes colonic tumorigenesis and activates colonic beta-catenin signaling pathway.

机构信息

Department of Biochemistry, Rush University, Chicago, IL, USA.

Biostatistics and Computational Biology, University of Rochester, Rochester, NY, USA.

出版信息

Oncogenesis. 2014 Jun 9;3(6):e105. doi: 10.1038/oncsis.2014.20.

Abstract

Salmonella infections can become chronic and increase the risk of cancer. The mechanisms by which specific Salmonella organisms contribute to cancer, however, are still unknown. Live and attenuated Salmonella are used as vectors to target cancer cells, but there have been no systematic studies of the oncogenic potential of chronic Salmonella infections in cancer models. AvrA, a pathogenic product of Salmonella, is inserted into host cells during infection and influences eukaryotic cell pathways. In the current study, we colonized mice with Salmonella AvrA-sufficient or AvrA-deficient Salmonella typhimirium strains and induced inflammation-associated colon cancer by azoxymethane/dextran sulfate sodium (AOM/DSS). We confirmed Salmonella persisted in the colon for up to 45 weeks. Salmonella was identified not only in epithelial cells on the colonic luminal surface and base of the crypts but also in invading tumors. Tumor incidence in the AvrA+infected group was 100% compared with 51.4% in the AOM/DSS group without bacterial gavage and 56.3% in mice infected with the AvrA- strain. Infection with AvrA+ strain also altered tumor distribution from the distal to proximal colon that might reflect changes in the microbiome. AvrA-expressing bacteria also upregulated beta-catenin signaling as assessed by decreased beta-catenin ubiquitination, increased nuclear beta-catenin and increased phosphorylated-beta-catenin (Ser552), a marker of proliferating stem-progenitor cells. Other β-catenin targets increased by AvrA included Bmi1, a cancer stem cell marker, matrix metalloproteinase-7, and cyclin D1. In summary, AvrA-expressing Salmonella infection activates β-catenin signals and enhances colonic tumorigenesis. Our findings provide important new mechanistic insights into how a bacterial protein targets proliferating stem-progenitor cells and contributes to cancer development. Our observations also raise a note of caution regarding the use of mutant Salmonella organisms as vectors for anti-cancer therapy. Finally, these studies could suggest biomarkers (such as AvrA level in gut) to assess cancer risk in susceptible individuals and infection-related dysregulation of β-catenin signaling in cancer.

摘要

沙门氏菌感染可能会变成慢性感染,并增加癌症的风险。然而,特定沙门氏菌生物体促进癌症的机制尚不清楚。活的和减毒的沙门氏菌被用作靶向癌细胞的载体,但在癌症模型中,尚未对慢性沙门氏菌感染的致癌潜力进行系统研究。沙门氏菌的一种致病产物 AvrA 在感染过程中插入宿主细胞,并影响真核细胞途径。在本研究中,我们用沙门氏菌 AvrA 充足或 AvrA 缺陷的鼠伤寒沙门氏菌菌株定植小鼠,并通过氧化偶氮甲烷/葡聚糖硫酸钠(AOM/DSS)诱导炎症相关的结肠癌。我们证实沙门氏菌在结肠中持续存在长达 45 周。沙门氏菌不仅存在于结肠腔表面的上皮细胞和隐窝底部,也存在于入侵的肿瘤中。与未进行细菌灌胃的 AOM/DSS 组(51.4%)和感染 AvrA-菌株的小鼠(56.3%)相比,AvrA+感染组的肿瘤发生率为 100%。感染 AvrA+菌株还改变了肿瘤的分布,从远端到近端结肠,这可能反映了微生物组的变化。AvrA 表达的细菌还通过降低β-连环蛋白的泛素化、增加核β-连环蛋白和增加磷酸化-β-连环蛋白(Ser552)来上调β-连环蛋白信号,后者是增殖性干细胞祖细胞的标志物。AvrA 上调的其他β-连环蛋白靶标包括癌症干细胞标志物 Bmi1、基质金属蛋白酶-7 和细胞周期蛋白 D1。总之,表达 AvrA 的沙门氏菌感染激活了β-连环蛋白信号并增强了结肠肿瘤发生。我们的研究结果为细菌蛋白靶向增殖性干细胞祖细胞并促进癌症发展的机制提供了重要的新见解。我们的观察结果还提醒人们注意使用突变沙门氏菌作为抗癌治疗载体的风险。最后,这些研究可能提示生物标志物(如肠道中的 AvrA 水平),以评估易感个体的癌症风险和癌症中β-连环蛋白信号的感染相关失调。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea96/4150214/63d432f7522c/oncsis201420f1.jpg

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