MicroRNA-149* suppresses hepatic inflammatory response through antagonizing STAT3 signaling pathway

Zhang, Qiqi; Su, Jia; Wang, Ziwei; Qi, Hui; Ge, Zeyong; Li, Zhijun; Chen, Weidong; Wang, Yandong

doi:10.18632/oncotarget.18541

Cited by 23 publications

(20 citation statements)

References 42 publications

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“…25,26 However, the biological significance of the down-regulation of miR-149* expression in diseases at the molecular level has not yet been fully elucidated. 13,23,27 Our recent publication supports a role for miR-149* in liver inflammation by negatively regulating STAT3-mediated cell signaling. 13 There has been growing evidence support that this chronic inflammation is a common origin of pathogenesis of hepatocellular carcinoma.…”

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confidence: 67%

miR-149* Suppresses Liver Cancer Progression by Down-Regulating Tumor Necrosis Factor Receptor 1–Associated Death Domain Protein Expression

Feng

Zhang

Nie

et al. 2020

The American Journal of Pathology

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Liver cancer is the third leading cause of cancer-related death worldwide. Herein, we show that miR-149* serves as a novel tumor suppressor for liver tumorigenesis. Mice with genetic deletion of miR-149* (miR-149* À/À mice), which caused loss of both miR-149 and miR-149*, were considerably more susceptible to acute liver injury and hepatic carcinogenesis induced by diethylnitrosamine than wild-type mice, accompanied by increased compensatory proliferation and up-regulated gene expression of certain inflammatory cytokines. miR-149* mimics dramatically impaired liver cancer cell proliferation and migration in vitro and blocked liver cancer progression in a xenograft model. Furthermore, miR-149* strongly suppressed NF-kB signaling and repressed tumor necrosis factor receptor type 1eassociated death domain protein expression in the NF-kB signaling pathway. These results reveal that miR-149*, as a novel liver tumor suppressor, may serve as a potential therapeutic target for liver cancer treatment.

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confidence: 67%

miR-149* Suppresses Liver Cancer Progression by Down-Regulating Tumor Necrosis Factor Receptor 1–Associated Death Domain Protein Expression

Feng

Zhang

Nie

et al. 2020

The American Journal of Pathology

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“…Its overexpression in macrophages has been linked to a significant decrease in MyD88 protein expression, as well as a reduced production of inflammatory mediators such as NF-κB, TNF-α, and IL-6 in response to infection or LPS stimulation ( 114 ). In addition, miR-149 inhibits the hepatic inflammatory response through STAT3-mediated signaling pathway ( 115 ). TNF-α induces endothelial activation through downregulation of miR-149, and its mimic transfection counteracted the TNF-α-induced expression of MMP-9, iNOS, and IL-6 ( 116 ).…”

Section: Mirnas and Inflammationmentioning

confidence: 99%

Anti-Inflammatory MicroRNAs and Their Potential for Inflammatory Diseases Treatment

et al. 2018

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Inflammation is a complicated biological and pathophysiological cascade of responses to infections and injuries, and inflammatory mechanisms are closely related to many diseases. The magnitude, the complicated network of pro- and anti-inflammatory factors, and the direction of the inflammatory response can impact on the development and progression of various disorders. The currently available treatment strategies often target the symptoms and not the causes of inflammatory disease and may often be ineffective. Since the onset and termination of inflammation are crucial to prevent tissue damage, a range of mechanisms has evolved in nature to regulate the process including negative and positive feedback loops. In this regard, microRNAs (miRNAs) have emerged as key gene regulators to control inflammation, and it is speculated that they are fine-tune signaling regulators to allow for proper resolution and prevent uncontrolled progress of inflammatory reactions. In this review, we discuss recent findings related to significant roles of miRNAs in immune regulation, especially the potential utility of these molecules as novel anti-inflammatory agents to treat inflammatory diseases. Furthermore, we discuss the possibilities of using miRNAs as drugs in the form of miRNA mimics or miRNA antagonists.

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“…The miRNA duplex is integrated into the “RNA-induced silencing complex” (RISC) after binding to the argonaute protein and a glycine tryptophan repeat-containing protein, where they bind to partial or full-complementary sequences in the 3’ or 5’ UTR of the target mRNA [ 28 , 29 ]. MiRNAs have been demonstrated to participate in the comprehensive network of gene regulation in the pathophysiological processes of many diseases [ 30 , 31 ].…”

Section: Biogenesis Of Non-coding Rnamentioning

confidence: 99%

Non-coding RNA: a potential biomarker and therapeutic target for sepsis

Zhang

Xia

et al. 2017

Oncotarget

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Sepsis, a syndrome of physiologic, pathologic, and biochemical abnormalities caused by an altered systemic host response to infection, has become the main cause of death among patients admitted to the intensive care units. Recently, genome-wide expression analysis revealed that over 80% of the essential genetic elements were altered in critically ill patients. Notably, non-coding RNAs, including microRNAs, long non-coding RNAs and circular RNAs, have been proven to play essential roles in innate immunity, mitochondrial dysfunction and organ dysfunction. In this review, we introduced the biogenesis of non-coding RNAs briefly and summed up different kinds of non-coding RNAs in regulation of sepsis, which could provide a more comprehensive understanding about pathogenesis of the disease. Additionally, we summarized the limitations of current biomarkers and then recommended some non-coding RNAs as novel potential biomarkers for sepsis and sepsis-induced organ dysfunction. Besides, we also introduced some problems and challenges that need to be overcome during the clinical application of non-coding RNAs. Future research should focus on elucidating their molecular mechanisms, particularly long non-coding RNAs as well as circular RNAs and sepsis, to further understanding of the disease process. With the in-depth understanding of the mechanism of sepsis, non-coding RNAs provide a new insight into sepsis and could become the novel therapeutic targets in the future.

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MicroRNA-149* suppresses hepatic inflammatory response through antagonizing STAT3 signaling pathway

Cited by 23 publications

References 42 publications

miR-149* Suppresses Liver Cancer Progression by Down-Regulating Tumor Necrosis Factor Receptor 1–Associated Death Domain Protein Expression

miR-149* Suppresses Liver Cancer Progression by Down-Regulating Tumor Necrosis Factor Receptor 1–Associated Death Domain Protein Expression

Anti-Inflammatory MicroRNAs and Their Potential for Inflammatory Diseases Treatment

Non-coding RNA: a potential biomarker and therapeutic target for sepsis

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