L‑fucose ameliorates the carcinogenic properties of <i>Fusobacterium nucleatum</i> in colorectal cancer

Duan, Caihan; Tang, Xueyuan; Qian, Wei; Fu, Xiaochao; Deng, Xiang‐Hua; Han, Chaoqun; Hou, Xiaohua

doi:10.3892/ol.2020.12404

Cited by 10 publications

(12 citation statements)

References 27 publications

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“…Previous studies revealed that L-fucose exhibited antitumor activity against various types of epithelial-derived cells of cancer, specifically colorectal cancer, gastric carcinoma, and hepatocellular carcinoma. [ 17 ] CCA is a typical bile duct epithelial-derived cancer that is intriguing and has been the focus of our research. Our study has once again broadened the scope of application of L-fucose to exert antitumor activity, and this study provides a good theoretical basis for L-fucose to enter clinical applications in the future.…”

Section: Discussionmentioning

confidence: 99%

L-Fucose inhibits the progression of cholangiocarcinoma by causing microRNA-200b overexpression

Zhu

Zheng

Hong

et al. 2023

Chinese Medical Journal

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Background: Cholangiocarcinoma (CCA) is a malignant biliary tract tumor with an extremely poor prognosis. There is an urgent demand to explore novel therapeutic strategies. L-fucose has been confirmed to participate in anti-inflammation and antitumor activities. However, the effect of L-fucose on the progression of CCA has not been well investigated. This study aimed to determine whether L-fucose induced the inhibition of CCA and its possible mechanism. Methods: The anti-growth activity was determined using Cell Counting Kit-8 assay, colony formation assays, Annexin Vfluorescein isothiocyanate/propidium iodide (FITC/PI) assay, and cell cycle analysis. The anti-metastasis activity was determined by wound healing, transwell, and invasion assays. The anti-angiogenesis activity was determined by tube formation and transwell assays. MicroRNAs that may be involved in the L-fucose-induced CCA inhibition was analyzed using bioinformatics methods. The preclinical therapeutic efficacy was mainly estimated by ultrasound in xenograft nude mouse models. Differences were analyzed via Student's t test or one-way analysis of variance. Results: L-Fucose induced apoptosis and G0/G1 cell cycle arrest, inhibited cell epithelial-mesenchymal transition of CCA cells, and additionally inhibited tube formation of human umbilical vein endothelial cells (HUVECs) in a dose-dependent manner, leading to a decrease in cell proliferation, metastasis, and angiogenesis. Mechanistically, L-fucose induced microRNA-200b (miR-200b) upregulation, and mitogen-activated protein kinase 7 (MAPK7) downregulation was found to be targeted by miR-200b, with decreased cell proliferation and metastasis. Additionally, phosphorylated signal transducer and activator of transcription 3 was found to be downregulated after L-fucose treatment. Finally, in vivo experiments in CCA xenograft models also confirmed the antitumor properties of L-fucose. Conclusion: L-Fucose inhibited the progression of CCA via the miR-200b/MAPK7 and signal transducer and activator of transcription 3 signaling pathways.

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Section: Discussionmentioning

confidence: 99%

L-Fucose inhibits the progression of cholangiocarcinoma by causing microRNA-200b overexpression

Zhu

Zheng

Hong

et al. 2023

Chinese Medical Journal

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“…Besides, Chen et al [ 31 ] have identified that Fn activates autophagy to promote CRC metastasis. It is worth mentioning that EMT is the most well-validated method by which Fn promotes CRC metastasis, and it has been discovered that the effect is enhanced when the MOI is increased[ 32 - 34 ]. EMT is a classical pathway promoting metastasis.…”

Section: Discussionmentioning

confidence: 99%

Salivary Fusobacterium nucleatum serves as a potential diagnostic biomarker for gastric cancer

Chen¹,

Zhang²,

Zhang³

et al. 2022

WJG

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BACKGROUND As one of the most common tumors, gastric cancer (GC) has a high mortality rate, since current examination approaches cannot achieve early diagnosis. Fusobacterium nucleatum (Fn) primarily colonized in the oral cavity, has been reported to be involved in the development of gastrointestinal tumor. Until now, little is known about the relationship between salivary Fn and GC. AIM To determine whether salivary Fn could be a biomarker to diagnose GC and explore the influence of Fn on GC cells. METHODS The abundance of Fn in saliva was quantified by droplet digital polymerase chain reaction in 120 GC patients, 31 atrophic gastritis (AG) patients, 35 non-AG (NAG) patients, 26 gastric polyp (GP) patients, and 20 normal controls (NC) from Qilu Hospital of Shandong University from January 2019 to December 2020. Receiver operating characteristic (ROC) curve analysis was performed to evaluate the diagnostic value of Fn as well as traditional serum tumor markers, including carcinoembryonic antigen (CEA), carbohydrate antigen (CA) 19-9, and CA72-4. Transwell assay and wound-healing assay were conducted to assess the influence of Fn infection on GC cells. The expression of epithelial-mesenchymal transition (EMT) markers was detected using western blot assay. RESULTS We found that the level of salivary Fn in GC patients was significantly increased compared with those in AG, NAG, and GP patients and NC ( P < 0.001). ROC curve analysis showed a favorable capability of Fn (73.33% sensitivity; 82.14% specificity; area under the curve: 0.813) in GC diagnosis, which was superior to that of CEA, CA19-9, CA72-4, ferritin, and sialic acid. The Fn level in saliva of GC patients was increased as the TNM stage increased. GC patients with lymph node metastasis had higher Fn levels than those without metastasis. Both transwell and wound-healing assays indicated that Fn infection promoted the migration and invasion of GC cells. Western blot analysis showed that Fn infection decreased the expression of E-cadherin and increased the expressions of N-cadherin, vimentin, and snail. CONCLUSION Fn abundance in saliva could be used as a promising biomarker to diagnose GC, and Fn infection could promote GC metastasis by accelerating the EMT process.

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“…Duan et al. revealed that L-fucose reversed the tumor-promoting properties of Fn by inhibiting its ability to activate jak-stat3 signaling and EMT in colon cancer cells in vitro ( Duan et al., 2021 ). Despite the lack of support from in vivo research data and rigorous validation of the mechanism, this finding is still eye-catching.…”

Section: Strategies For Crc Prevention and Treatment By Anti-fnmentioning

confidence: 99%

Fusobacterium nucleatum and colorectal cancer: From phenomenon to mechanism

Wang

Tao

et al. 2022

Front. Cell. Infect. Microbiol.

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Colorectal cancer(CRC) is the third most frequent malignant tumor. The gut microbiome acts as a vital component of CRC etiology. Fusobacterium nucleatum(Fn) is a key member of colorectal cancer-associated bacteria. But we lack a systematic and in-depth understanding on its role in CRC evolution. In this article, We reviewed the abundance changes and distribution of Fn in CRC occurrence and development, potential effect of Fn in the initiation of CRC, the source of intratumoral Fn and the cause of its tropism to CRC. In addition, We described the mechanism by which Fn promotes the malignant biological behavior of CRC, affects CRC response to therapy, and shapes the tumor immune microenvironment in great detail. Based on the relationship between Fn and CRC, we proposed strategies for CRC prevention and treatment, and discussed the feasibility and limitations of specific cases, to gain insights into further basic and clinical research in the future.

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L‑fucose ameliorates the carcinogenic properties of Fusobacterium nucleatum in colorectal cancer

Cited by 10 publications

References 27 publications

L-Fucose inhibits the progression of cholangiocarcinoma by causing microRNA-200b overexpression

L-Fucose inhibits the progression of cholangiocarcinoma by causing microRNA-200b overexpression

Salivary Fusobacterium nucleatum serves as a potential diagnostic biomarker for gastric cancer

Fusobacterium nucleatum and colorectal cancer: From phenomenon to mechanism

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