“…Wanget al [11] also revealed that butyrate modulated the activity of the transforming growth factor-beta 1 TGF-β1/Smad3 signaling pathway, which is a cytokine that plays a crucial role in regulating cell growth, differentiation, apoptosis, and immune response. It exerts its effects by binding to cell surface receptors, activating downstream signaling pathways, including the Smad proteins [114]. The TGF-β1/Smad3 signaling pathway is indeed relevant to lymphoma, and its dysregulation can contribute to tumor development and progression [114].…”
Section: Et Al [104]mentioning
confidence: 99%
“…It exerts its effects by binding to cell surface receptors, activating downstream signaling pathways, including the Smad proteins [114]. The TGF-β1/Smad3 signaling pathway is indeed relevant to lymphoma, and its dysregulation can contribute to tumor development and progression [114]. However, further research is needed to confirm these findings and to determine the interactions of butyrate with standard chemotherapy [11], as well as its impact on lymphoma.…”
Recent research has implicated the gut microbiota in the development of lymphoma. Dysbiosis of the gut microbial community can disrupt the production of gut microbial metabolites, thereby impacting host physiology and potentially contributing to lymphoma. Dysbiosis-driven release of gut microbial metabolites such as lipopolysaccharides can promote chronic inflammation, potentially elevating the risk of lymphoma. In contrast, gut microbial metabolites, such as short-chain fatty acids, have shown promise in preclinical studies by promoting regulatory T-cell function, suppressing inflammation, and potentially preventing lymphoma. Another metabolite, urolithin A, exhibited immunomodulatory and antiproliferative properties against lymphoma cell lines in vitro. While research on the role of gut microbial metabolites in lymphoma is limited, this article emphasizes the need to comprehend their significance, including therapeutic applications, molecular mechanisms of action, and interactions with standard chemotherapies. The article also suggests promising directions for future research in this emerging field of connection between lymphoma and gut microbiome.
“…Wanget al [11] also revealed that butyrate modulated the activity of the transforming growth factor-beta 1 TGF-β1/Smad3 signaling pathway, which is a cytokine that plays a crucial role in regulating cell growth, differentiation, apoptosis, and immune response. It exerts its effects by binding to cell surface receptors, activating downstream signaling pathways, including the Smad proteins [114]. The TGF-β1/Smad3 signaling pathway is indeed relevant to lymphoma, and its dysregulation can contribute to tumor development and progression [114].…”
Section: Et Al [104]mentioning
confidence: 99%
“…It exerts its effects by binding to cell surface receptors, activating downstream signaling pathways, including the Smad proteins [114]. The TGF-β1/Smad3 signaling pathway is indeed relevant to lymphoma, and its dysregulation can contribute to tumor development and progression [114]. However, further research is needed to confirm these findings and to determine the interactions of butyrate with standard chemotherapy [11], as well as its impact on lymphoma.…”
Recent research has implicated the gut microbiota in the development of lymphoma. Dysbiosis of the gut microbial community can disrupt the production of gut microbial metabolites, thereby impacting host physiology and potentially contributing to lymphoma. Dysbiosis-driven release of gut microbial metabolites such as lipopolysaccharides can promote chronic inflammation, potentially elevating the risk of lymphoma. In contrast, gut microbial metabolites, such as short-chain fatty acids, have shown promise in preclinical studies by promoting regulatory T-cell function, suppressing inflammation, and potentially preventing lymphoma. Another metabolite, urolithin A, exhibited immunomodulatory and antiproliferative properties against lymphoma cell lines in vitro. While research on the role of gut microbial metabolites in lymphoma is limited, this article emphasizes the need to comprehend their significance, including therapeutic applications, molecular mechanisms of action, and interactions with standard chemotherapies. The article also suggests promising directions for future research in this emerging field of connection between lymphoma and gut microbiome.
“…Wang et al (2020) also revealed that butyrate modulated the activity of the transforming growth factor-beta 1 TGF-β1/Smad3 signalling pathway, which is a cytokine that plays a crucial role in regulating cell growth, differentiation, apoptosis, and immune response. It exerts its effects by binding to cell surface receptors, activating downstream signalling pathways, including the Smad proteins (Chen et al, 2023). The TGF-β1/Smad3 signalling pathway is indeed relevant to lymphoma and its dysregulation can contribute to tumour development and progression (Chen et al, 2023).…”
Section: Scfasmentioning
confidence: 99%
“…It exerts its effects by binding to cell surface receptors, activating downstream signalling pathways, including the Smad proteins (Chen et al, 2023). The TGF-β1/Smad3 signalling pathway is indeed relevant to lymphoma and its dysregulation can contribute to tumour development and progression (Chen et al, 2023). However, further research is needed to confirm these findings and to determine the interactions of butyrate with standard chemotherapy (Wang et al, 2020) as well as its impact on lymphoma.…”
Recent research has implicated the gut microbiota in the development of lymphoma. Dysbiosis of the gut microbial community can disrupt the production of gut microbial metabolites, thereby impacting host physiology and potentially contributing to lymphoma. Dysbiosis-driven release of gut microbial metabolites such as lipopolysaccharides can promote chronic inflammation, potentially elevating the risk of lymphoma. In contrast, gut microbial metabolites, such as short-chain fatty acids, have shown promise in preclinical studies by promoting regulatory T-cell function, suppressing inflammation, and preventing lymphoma. Another metabolite, urolithin A, exhibited immunomodulatory and antiproliferative properties against lymphoma cell lines in vitro. While research on the role of gut microbial metabolites in lymphoma is limited, this article emphasizes the need to comprehend their significance, including therapeutic applications, molecular mechanisms of action, and interactions with standard chemotherapies. The article also suggests promising directions for future research in this emerging lymphoma and gut microbiome investigation field.
Protein post-translational modification (PTM) is a covalent process that occurs in proteins during or after translation through the addition or removal of one or more functional groups, and has a profound effect on protein function. Glycosylation is one of the most common PTMs, in which polysaccharides are transferred to specific amino acid residues in proteins by glycosyltransferases. A growing body of evidence suggests that glycosylation is essential for the unfolding of various functional activities in organisms, such as playing a key role in the regulation of protein function, cell adhesion and immune escape. Aberrant glycosylation is also closely associated with the development of various diseases. Abnormal glycosylation patterns are closely linked to the emergence of various health conditions, including cancer, inflammation, autoimmune disorders, and several other diseases. However, the underlying composition and structure of the glycosylated residues have not been determined. It is imperative to fully understand the internal structure and differential expression of glycosylation, and to incorporate advanced detection technologies to keep the knowledge advancing. Investigations on the clinical applications of glycosylation focused on sensitive and promising biomarkers, development of more effective small molecule targeted drugs and emerging vaccines. These studies provide a new area for novel therapeutic strategies based on glycosylation.
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