Noncoding RNAs: Master Regulators of Inflammatory Signaling

Chew, Chen Li; Conos, Stephanie A.; Unal, Bilal; Tergaonkar, Vinay

doi:10.1016/j.molmed.2017.11.003

Cited by 147 publications

(116 citation statements)

References 151 publications

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“…They have been identified as splicing activities or transcriptional regulators, scaffolds of proteins, miRNA sponges, and protect mRNA targets from cleavage and translation repression induced by miRNAs. Moreover, many circRNAs are tissue‐specifically expressed, highly conserved, and can be detected in many kinds of body fluids . circRNA_100782 was markedly upregulated in pancreatic ductal adenocarcinoma tissue and regulated BxPC3 pancreatic cancer cells proliferation by acting as miR‐124 sponge through the IL6–STAT3 pathway .…”

Section: Introductionmentioning

confidence: 99%

“…Moreover, many cir-cRNAs are tissue-specifically expressed, highly conserved, and can be detected in many kinds of body fluids. [40][41][42][43][44] circRNA_100782 was markedly upregulated in pancreatic ductal adenocarcinoma tissue and regulated BxPC3 pancreatic cancer cells proliferation by acting as miR-124 sponge through the IL6-STAT3 pathway. 45 Functional experiments revealed circRNA_010567 silencing could upregulate miR-141 and downregulate TGF-β1 expression, play an important regulatory role in the diabetic mice myocardial fibrosis model, and suppress fibrosis-associated protein resection in cardiac fibroblasts.…”

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confidence: 99%

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MicroRNAs play an essential role in autophagy regulation in various disease phenotypes

et al. 2019

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Autophagy is a highly conserved catabolic process and fundamental biological process in eukaryotic cells. It recycles intracellular components to provide nutrients during starvation and maintains quality control of organelles and proteins. In addition, autophagy is a well‐organized homeostatic cellular process that is responsible for the removal of damaged organelles and intracellular pathogens. Moreover, it also modulates the innate and adaptive immune systems. Micro ribonucleic acids (microRNAs) are a mature class of post‐transcriptional modulators that are widely expressed in tissues and organs. And, it can suppress gene expression by targeting messenger RNAs for translational repression or, at a lesser extent, degradation. Research indicates that microRNAs regulate autophagy through different pathways, playing an essential role in the treatment of various diseases. It is an important regulator of fundamental cellular processes such as proliferation, autophagy, and cell apoptosis. In this review article, we first review the current knowledge of autophagy and the function of microRNAs. Then, we summarize the mechanism of autophagy and the signaling pathways related to autophagy by citing at least the main proteins involved in the different phases of the process. Second, we introduce other members of RNA and report some examples in various pathologies. Finally, we review the current literature regarding microRNA‐based therapies for cancer, atherosclerosis, cardiac disease, tuberculosis, and viral diseases. MicroRNAs can cause autophagy upregulation or downregulation by targeting genes or affecting autophagy‐related signaling pathways. Therefore, the microRNAs have a huge potential in autophagy regulation, and it is the function as diagnostic and prognostic markers.

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Section: Introductionmentioning

confidence: 99%

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confidence: 99%

MicroRNAs play an essential role in autophagy regulation in various disease phenotypes

et al. 2019

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“…Hong et al [109], via RNA-seq, pinpointed differences between the inflamed and non-inflamed intestinal mucosa of CD patients and healthy controls. Of high interest in recent years is the study of noncoding RNAs and their role, as depicted in reviews and original articles [110][111][112][113][114][115][116].…”

Section: Transcriptomics In Ibdmentioning

confidence: 99%

Systems biology in inflammatory bowel diseases: on the way to precision medicine

Dovrolis

Filidou

Kolios

2019

aog

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Inflammatory bowel diseases (IBD) are chronic and recurrent inflammatory disorders of the gastrointestinal tract. The elucidation of their etiopathology requires complex and multiple approaches. Systems biology has come to fulfill this need in approaching the pathogenetic mechanisms of IBD and its etiopathology, in a comprehensive way, by combining data from different scientific sources. In combination with bioinformatics and network medicine, it uses principles from computer science, mathematics, physics, chemistry, biology, medicine and computational tools to achieve its purposes. Systems biology utilizes scientific sources that provide data from omics studies (e.g., genomics, transcriptomics, etc.) and clinical observations, whose combined analysis leads to network formation and ultimately to a more integrative image of disease etiopathogenesis. In this review, we analyze the current literature on the methods and the tools utilized by systems biology in order to cover an innovative and exciting field: IBD-omics.

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“…as the TNF receptor (TNFR) and innate immune receptors such as Toll-like receptors (TLR) (Chew et al 2018;Correa et al 2005) (Fig. 1b).…”

Section: Introductionmentioning

confidence: 99%

“…This leads to the consequent activation of IκB kinase (IKK) complex, which phosphorylates IκBα, triggering its ubiquitin-dependent degradation and the consequent release of p50-RelA heterodimers into the nucleus, where they activate the transcription of NF-κB target genes ( Fig. 1b) (Chew et al 2018).…”

Section: Introductionmentioning

confidence: 99%

Inflammation-associated genomic instability in cancer

Pua

Chew

Lane

et al. 2019

GENOME INSTAB. DIS.

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Inflammation is essential in protecting us against foreign pathogens. However when left unchecked, it becomes chronic inflammation, a potential precursor to carcinogenesis. While inflammatory signalling provides pro-survival stimuli, it also causes genomic instability and allows mutant cells to escape cell cycle arrest and apoptosis. This occurs through the release of reactive oxygen/nitrogen species (ROS/RNS), the increased expression of activation-induced cytidine deaminase (AID), inhibition of p53 function and the reactivation of TERT expression. Because chronic inflammation can ultimately lead to genomic instability, there is a need to target chronic inflammation, through the suppression of effector pathways with biologics or small molecules. More recently, therapies have also focused on stimulating physiological resolution, which offers a promising, tissue-specific alternative. As we better understand the triggers of chronic inflammation, therapies can be more specific, without compromising the overall functions of our immune system.

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Noncoding RNAs: Master Regulators of Inflammatory Signaling

Cited by 147 publications

References 151 publications

MicroRNAs play an essential role in autophagy regulation in various disease phenotypes

MicroRNAs play an essential role in autophagy regulation in various disease phenotypes

Systems biology in inflammatory bowel diseases: on the way to precision medicine

Inflammation-associated genomic instability in cancer

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