Fusobacterium nucleatum promotes colorectal cancer metastasis by excretion of miR-122-5p from cells via exosomes

Zhang, Mengjiao; Wang, Yifeng; Yu, Longchen; Zhang, Yanli; Wang, Yanlei; Shang, Ziqi; Xin, Yiwei; Li, Xinyang; Ning, Nannan; Zhang, Yi; Zhang, Xin

doi:10.1016/j.isci.2023.107686

Cited by 5 publications

(4 citation statements)

References 39 publications

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“…Besides, F. nucleatum was found to produce a novel virulence molecule, DNA hunger/stationary phase protective proteins (Dps), which stimulates macrophages to secrete chemokines C-C motif chemokine ligand (CCL) 2/7, thus regulating the expression of relevant factors involved in the EMT process to promote tumour metastasis [ 44 ]. In addition, F. nucleatum also regulates the expression of non-coding RNAs, including long non-coding RNAs (lncRNAs) and microRNAs (miRNAs), to mediate the EMT process in CRC cells [ 45 , 46 ]. LncRNAs are RNAs longer than 200 nucleotides, and miRNAs are 20- to 22-nucleotide-single-stranded RNAs with a highly stable structure [ 47 , 48 ].…”

Section: Mechanisms Underlying the Promotion Of Crc Metastasis By Imb...mentioning

confidence: 99%

“…F. nucleatum upregulates the expression of the endogenous retroviral-associated adenocarcinoma lncRNA ( EVADR ), and then makes the elevated EVADR a modular scaffold of Y-box binding protein 1 (YBX1), an RNA-binding protein that is capable of stimulating the production of EMT-associated factors, to directly enhances the translation of EMT-associated factors, such as Snail, Slug and Zeb1, thereby inducing EMT [ 45 , 50 ]. F. nucleatum infection reduces the level of the intracellular tumour suppressor gene miR-122-5p to cause overexpression of its downstream target α1,6-Fucosyltransferase (FUT8), which activates the transforming growth factor-β1 (TGF-β1)/Smads signaling pathway, inducing a decrease in E-cadherin levels while contributing to an increase in N-cadherin, Vimentin, Snail and Slug levels to promote EMT [ 46 ]. However, it is widely acknowledged that individual RNA is not expected to have a significant impact on CRC progression.…”

Section: Mechanisms Underlying the Promotion Of Crc Metastasis By Imb...mentioning

confidence: 99%

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Role of imbalanced gut microbiota in promoting CRC metastasis: from theory to clinical application

Fan,

Zhou,

Zhang

et al. 2024

Cell Commun Signal

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Metastasis poses a major challenge in colorectal cancer (CRC) treatment and remains a primary cause of mortality among patients with CRC. Recent investigations have elucidated the involvement of disrupted gut microbiota homeostasis in various facets of CRC metastasis, exerting a pivotal influence in shaping the metastatic microenvironment, triggering epithelial-mesenchymal transition (EMT), and so on. Moreover, therapeutic interventions targeting the gut microbiota demonstrate promise in enhancing the efficacy of conventional treatments for metastatic CRC (mCRC), presenting novel avenues for mCRC clinical management. Grounded in the “seed and soil” hypothesis, this review consolidates insights into the mechanisms by which imbalanced gut microbiota promotes mCRC and highlights recent strides in leveraging gut microbiota modulation for the clinical prevention and treatment of mCRC. Emphasis is placed on the considerable potential of manipulating gut microbiota within clinical settings for managing mCRC.

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Section: Mechanisms Underlying the Promotion Of Crc Metastasis By Imb...mentioning

confidence: 99%

Section: Mechanisms Underlying the Promotion Of Crc Metastasis By Imb...mentioning

confidence: 99%

Role of imbalanced gut microbiota in promoting CRC metastasis: from theory to clinical application

Fan,

Zhou,

Zhang

et al. 2024

Cell Commun Signal

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“…MiR-122-5p can inhibit the expression of FUT8, but its expression is low in cancer [69]. While Mengjiao Zhang et al explained the mechanism of the reduction of tumor-suppressive miR-122-5p in CRC infected by fusobacterium nucleatum, this infection would trigger the secretion of intracellular miR-122-5p into exosomes via an RNA-binding protein-hnRNPA2B1 [106].…”

Section: At the Post-transcriptional Levelmentioning

confidence: 99%

The Multifaceted Role of FUT8 in Tumorigenesis: From Pathways to Potential Clinical Applications

Shi,

Nan,

Liu

2024

IJMS

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FUT8, the sole glycosyltransferase responsible for N-glycan core fucosylation, plays a crucial role in tumorigenesis and development. Aberrant FUT8 expression disrupts the function of critical cellular components and triggers the abnormality of tumor signaling pathways, leading to malignant transformations such as proliferation, invasion, metastasis, and immunosuppression. The association between FUT8 and unfavorable outcomes in various tumors underscores its potential as a valuable diagnostic marker. Given the remarkable variation in biological functions and regulatory mechanisms of FUT8 across different tumor types, gaining a comprehensive understanding of its complexity is imperative. Here, we review how FUT8 plays roles in tumorigenesis and development, and how this outcome could be utilized to develop potential clinical therapies for tumors.

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“…Similarly, in F. nucleatum -infected CRC cells we observed that the RNA-binding protein hnRNPA2B1 mediated the secretion of oncogene miR-122-5P by F. nucleatum into exosomes, leading to the downregulation of its expression in CRC cells and in turn an upregulation of FUT8 expression promoting the migratory and proliferative capacities of tumor cells. Moreover, it has been further revealed that F. nucleatum activated the TGF-β1/Smads signaling pathway by regulating the miRNA-122-5p/FUT8 axis to promote EMT, resulting in tumorigenesis and development[ 36 ].…”

Section: Mechanisms Of Carcinogenesis Of F Nucleatummentioning

confidence: 99%

Application of Fusobacterium nucleatum as a biomarker in gastrointestinal malignancies

Yu,

Li,

Xin

et al. 2024

World J Gastrointest Oncol

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The morbidity and mortality of gastrointestinal (GI) malignancies are among the highest in the world, posing a serious threat to human health. Because of the insidious onset of the cancer, it is difficult for patients to be diagnosed at an early stage, and it rapidly progresses to an advanced stage, resulting in poor treatment and prognosis. Fusobacterium nucleatum (F. nucleatum ) is a gram-negative, spore-free anaerobic bacterium that primarily colonizes the oral cavity and is implicated in the development of colorectal, esophageal, gastric, and pancreatic cancers via various intricate mechanisms. Recent development in novel research suggests that F. nucleatum may function as a biomarker in GI malignancies. Detecting the abundance of F. nucleatum in stool, saliva, and serum samples of patients may aid in the diagnosis, risk assessment, and prognosis monitoring of GI malignancies. This editorial systematically describes the biological roles and mechanisms of F. nucleatum in GI malignancies focusing on the application of F. nucleatum as a biomarker in the diagnosis and prognosis of GI malignancies to promote the clinical translation of F. nucleatum and GI tumors-related research.

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Fusobacterium nucleatum promotes colorectal cancer metastasis by excretion of miR-122-5p from cells via exosomes

Cited by 5 publications

References 39 publications

Role of imbalanced gut microbiota in promoting CRC metastasis: from theory to clinical application

Role of imbalanced gut microbiota in promoting CRC metastasis: from theory to clinical application

The Multifaceted Role of FUT8 in Tumorigenesis: From Pathways to Potential Clinical Applications

Application of Fusobacterium nucleatum as a biomarker in gastrointestinal malignancies

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