Potential role of Escherichia coli DNA mismatch repair proteins in colon cancer

Khan, Shahanavaj

doi:10.1016/j.critrevonc.2015.05.002

Cited by 38 publications

(44 citation statements)

References 82 publications

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“…We suspect it may be correlated with the abnormal gut environment induced by colitis and CRC. The abundance of Escherichia and Enterococcus , which are both opportunistic pathogens, was increased in CAC patients [49–50]. Consistent with these data, we found that the abundance of Enterococcus was also increased in CACM compared to CK mice (0.011% vs. 6.9E-4%), and was below the detection limit in CIH mice.…”

Section: Discussionsupporting

confidence: 86%

Isoliquiritigenin decreases the incidence of colitis-associated colorectal cancer by modulating the intestinal microbiota

Deng

et al. 2016

Oncotarget

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Imbalances in intestinal bacteria correlate with colitis-associated colorectal cancer (CAC). Traditional Chinese medicines have been used to adjust the gut microbiota, and isoliquiritigenin (ISL), a flavonoid extracted from licorice, has shown antitumor efficacy. In this study, the effects of ISL on CAC development and the gut microbiota were evaluated using an azoxymethane and dextran sulphate sodium (AOM/DSS)-induced mouse model of CAC (CACM). Histopathological analysis suggested that ISL reduced tumor incidence in vivo. Moreover, high-throughput sequencing and terminal restriction fragment length polymorphism (T-RFLP) studies of the bacterial 16S rRNA gene revealed that the structure of the gut microbial community shifted significantly following AOM/DSS treatment, and that effect was alleviated by treatment with high-dose ISL (150 mg/kg). Compared to the microbiota in the control mice (CK), the levels of Bacteroidetes decreased and the levels of Firmicutes increased during CAC development. ISL reversed the imbalance at the phylum level and altered the familial constituents of the gut microbiota. Specifically, the abundance of Helicobacteraceae increased after treatment with high-dose ISL, while the abundance of Lachnospiraceae and Rikenellaceae decreased. At the genus level, ISL reduced the abundance of opportunistic pathogens (Escherichia and Enterococcus), and increased the levels of probiotics, particularly butyrate-producing bacteria (Butyricicoccus, Clostridium, and Ruminococcus). Thus, ISL protects mice from AOM/DSS-induced CAC, and ISL and the gut microbiota may have synergistic anti-cancer effects.

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Section: Discussionsupporting

confidence: 86%

Isoliquiritigenin decreases the incidence of colitis-associated colorectal cancer by modulating the intestinal microbiota

Deng

et al. 2016

Oncotarget

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“…Alterations in the MutS or MutL complexes of mammalian cells may be associated with EPEC pathogenesis and the development of CRC. The MMR proteins of E. coli have been considered as potential therapeutic targets and early detection biomarkers for CRC 131 . The role of gut microbiota in the development of human CRC is influenced by diet and inflammation 132 .…”

Section: General Aspects Of the Unfolded Protein Responsementioning

confidence: 99%

New frontiers in the treatment of colorectal cancer: Autophagy and the unfolded protein response as promising targets

et al. 2017

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Colorectal cancer (CRC), despite numerous therapeutic and screening attempts, still remains a major life-threatening malignancy. CRC etiology entails both genetic and environmental factors. Macroautophagy/autophagy and the unfolded protein response (UPR) are fundamental mechanisms involved in the regulation of cellular responses to environmental and genetic stresses. Both pathways are interconnected and regulate cellular responses to apoptotic stimuli. In this review, we address the epidemiology and risk factors of CRC, including genetic mutations leading to the occurrence of the disease. Next, we discuss mutations of genes related to autophagy and the UPR in CRC. Then, we discuss how autophagy and the UPR are involved in the regulation of CRC and how they associate with obesity and inflammatory responses in CRC. Finally, we provide perspectives for the modulation of autophagy and the UPR as new therapeutic options for CRC treatment.

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“…Studies have shown that 40-50% of human colorectal cancer is caused by the activity of KRAS protein expression, and inhibition of KRAS expression can inhibit tumor growth [51][52][53]. In recent years, a hypothesis that adherent A/E E. coli has a connection with colorectal carcinogenesis in humans has been put forth [54][55][56]. It has been shown that EPEC infection can cause phenomena such as dramatically enhancing the spontaneous mutation frequency in host cells, inducing mismatch repair (MMR) protein dysfunction and increasing the levels of host reactive oxygen species, which were considered to be symbols of tumorigenesis.…”

Section: Espf May Induce Colitis and Colorectal Carcinogenesis Through mentioning

confidence: 99%

Screening for Host Proteins Interacting with Escherichia Coli O157:H7 EspF using Bimolecular Fluorescence Complementation

Hua

Wang

et al. 2017

Future Microbiol.

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Aim:To screen host proteins that interact with enterohemorrhagic Escherichia coli O157:H7 EspF. Materials & methods: Flow cytometry and high-throughput sequencing were used to screen interacting proteins. Molecular function, biological processes and Kyoto Encyclopedia of Genes and Genomes pathways were studied using the DAVID online tool. Glutathione S-transferase pull down and dot blotting were used to verify the interactions. Results: 293 host proteins were identified to associate with EspF. They were mainly enriched in RNA splicing (p = 0.005), ribosome structure (p = 0.012), and involved in 109 types of signaling pathways. SNX9 and ANXA6 were confirmed to interact with EspF. Conclusion: EspF interacts with ANXA6; they may form a complex to manipulate the process of phagocytosis; EspF plays a highlighted pathogenic role in enterohemorrhagic E. coli infection process. Enterohemorrhagic Escherichia coli (EHEC) O157:H7 is an important food-borne causative agent in sporadic outbreaks of illness such as diarrhea, hemorrhagic colitis and hemolytic-uremic syndrome. Severe symptoms may even lead to death [1][2][3][4]. Research into EHEC has mainly explored the development of attaching and effacing (A/E) intestinal lesions and the secretion of Shiga toxin in EHEC infection [5][6][7]. The protein EspF is one of the multifunctional effectors of A/E lesions induced by EHEC and enteropathogenic E. coli (EPEC). EspF participates in a number of damage processes in host cells, targeting mitochondria and nucleoli [6,8] and disrupting the tight junctions (TJs) of intestinal epithelial cells [9], leading to cytoskeletal rearrangements, actin polymerization and pedestal formation [10]. EspF thus emerges as the 'Swiss army knife' of a bacterial pathogen [11,12]. EHEC O157:H7 employs a type-III secretion system to export toxic factors and effector proteins to host cells after adhering to the brush border of epithelial cells [5,[13][14]. The production of virulence factors, subsequent invasion and diffusion, and the interaction of effector proteins with host proteins are key steps in EHEC O157:H7 pathogenesis. The mechanism by which EspF breaks through the intestinal epithelial barrier into host cells, the host proteins that EspF interacts with, and how cellular damage, and even apoptosis, result remain unclear. Studying the pathogen-host interaction process will increase the emerging knowledge about EHEC O157:H7 pathogenesis.The EspF protein has been shown to induce apoptosis after 'injection' into host cells [1]. The N-terminal (1-73 amino acids [aa]) of this approximately 27 kDa protein contains a secretory signal (1-20 aa), a mitochondrialtargeting signal (1-24 aa) and a nucleolar-targeting domain (21-74 aa); 73-248 aa consists of four proline-rich repeats (PRRs), each containing a eukaryotic cell sorting nexin 9 (SNX9) protein-binding site SH3 motif, an

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Potential role of Escherichia coli DNA mismatch repair proteins in colon cancer

Cited by 38 publications

References 82 publications

Isoliquiritigenin decreases the incidence of colitis-associated colorectal cancer by modulating the intestinal microbiota

Isoliquiritigenin decreases the incidence of colitis-associated colorectal cancer by modulating the intestinal microbiota

New frontiers in the treatment of colorectal cancer: Autophagy and the unfolded protein response as promising targets

Screening for Host Proteins Interacting with Escherichia Coli O157:H7 EspF using Bimolecular Fluorescence Complementation

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