The STAT3-regulated long non-coding RNA Lethe promote the HCV replication

Xiong, Yong; Yuan, Jing; Zhang, Changjiang; Zhu, Yan; Kuang, Xuemei; Lin, Lih-Yuan; Wang, Xiaohong

doi:10.1016/j.biopha.2015.04.019

Cited by 24 publications

(26 citation statements)

References 24 publications

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“…It is highly expressed in both knee and hip osteoarthritis chondrocytes when compared with non-osteoarthritic samples, suggesting a possible role in mediating inflammation-driven cartilage damage in osteoarthritis (54). Lethe is found to enhance the replication of the hepatitis C virus by suppressing interferon-stimulated gene expression after a type 1 interferon response (69). NKILA is found to serve as a tumor suppressor through a negative feedback loop of NF-B and inhibits breast cancer progression and metastasis (50).…”

Section: Lncrnas and Pathogenesis Of Inflammatory Diseasementioning

confidence: 99%

Long non-coding RNAs (lncRNAs) and their transcriptional control of inflammatory responses

Mathy

Chen

2017

Journal of Biological Chemistry

213

162

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Edited by George M. Carman Long non-coding RNAs (lncRNAs) have emerged as potential key regulators of the inflammatory response, particularly by modulating the transcriptional control of inflammatory genes. lncRNAs may act as an enhancer or suppressor to inflammatory transcription, function as scaffold molecules through interactions with RNA-binding proteins in chromatin remodeling complexes, and modulate dynamic and epigenetic control of inflammatory transcription in a gene-specific and time-dependent fashion. Here, we will review recent literature regarding the role of lncRNAs in transcriptional control of inflammatory responses. Better understanding of lncRNA regulation of inflammation will provide novel targets for the development of new therapeutic strategies.Because of the potentially destructive nature of the inflammatory response, the expression of inflammation-related genes is finely regulated at multiple levels, including transcription, mRNA processing, translation, phosphorylation, and degradation. Transcription represents an essential, and often the most important, regulatory determinant of the inflammation process. Many signaling pathways and transcription factors are involved in the inflammatory response, including the transcription factor nuclear factor-B (NF-B), 2 MAPK, and JAK/ STAT pathways, together controlling a multitude of inflammatory response genes (1, 2). Upon activation, these pathways directly activate and induce the expression of a limited set of transcription factors that promote the transcription of inflammatory genes. Whereas the mechanisms of initial activation and subsequent nuclear translocation of associated transcription factors for these signaling pathways are well-characterized, how the transcription of inflammatory genes is finely controlled in the nucleus to ensure that each individual gene is transcribed at the "right" place at the "right" time remains elusive. Perhaps this can be best represented by the inflammatory transcription induced by NF-B. The NF-B signaling cascade can be activated by inflammatory signals, including LPS, TNF-␣, IL-1␤, and reactive oxygen species, among others; many Toll-like receptors (TLRs) also activate NF-B (3-8).Prior to an activating signal, NF-B dimers are sequestered in the cytoplasm and held inactive by association with I B proteins (9). Activating stimuli cause I B degradation (10, 11), and consequently, free NF-B dimers translocate to the nucleus, bind to B sites, and promote gene transcription (12). Common targets of NF-B include inflammatory cytokines, chemokines, adhesion molecules, cytoprotective proteins, and proteins regulating cell differentiation, proliferation, and survival (13,14). In addition to its initial cytoplasmic activation, both the recruitment of NF-B to target genes in the nuclei and NF-B-induced transcriptional events after recruitment are finely controlled events to ensure proper transactivation of NF-B target genes (15). Indeed, several waves of gene transcription have been demonstrated in macrophages following LP...

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Section: Lncrnas and Pathogenesis Of Inflammatory Diseasementioning

confidence: 99%

Long non-coding RNAs (lncRNAs) and their transcriptional control of inflammatory responses

Mathy

Chen

2017

Journal of Biological Chemistry

213

162

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“…Although the best example of a pseudogene functioning as an lncRNA may come from X‐inactive specific transcript, which is essential for dosage compensation and X chromosome inactivation in female mammals, Lethe provides the first evidence that a pseudogene is capable of functioning as an lncRNA to regulate inflammatory signalling. Interestingly, Lethe can also be induced by signal transducer and activator of transcription 3 (STAT3), and elevated expression of Lethe promotes hepatitis C virus replication by down‐regulating type I interferon response . This seems logical considering the fact that the p65 subunit of NF‐ κ B could physically associate with STAT3, facilitating NF‐ κ B recruitment to STAT3 promoters and vice versa …”

Section: Lncrnas Interact With Nf‐κb or Its Transcriptsmentioning

confidence: 99%

Long non‐coding RNA: a versatile regulator of the nuclear factor‐κB signalling circuit

Mao

Mookhtiar

2017

Immunology

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SummaryThe nuclear factor-jB (NF-jB) family of transcription factors play an essential role for the regulation of inflammatory responses, immune function and malignant transformation. Aberrant activity of this signalling pathway may lead to inflammation, autoimmune diseases and oncogenesis. Over the last two decades great progress has been made in the understanding of NF-jB activation and how the response is counteracted for maintaining tissue homeostasis. Therapeutic targeting of this pathway has largely remained ineffective due to the widespread role of this vital pathway and the lack of specificity of the therapies currently available. Besides regulatory proteins and microRNAs, long non-coding RNA (lncRNA) is emerging as another critical layer of the intricate modulatory architecture for the control of the NF-jB signalling circuit. In this paper we focus on recent progress concerning lncRNA-mediated modulation of the NF-jB pathway, and evaluate the potential therapeutic uses and challenges of using lncRNAs that regulate NF-jB activity.

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“…The main risk factors for developing HCC are well-known and include cirrhosis, hepatitis B virus (HBV) or hepatitis C virus (HCV) infection, alcohol abuse, aflatoxin B1 ingestion, and non-alcoholic steatohepatitis. Major pathways with frequent mutations in HCC include the telomere maintenance pathway, the cell cycle pathway, the WNT-β-catenin pathway, the epigenetic remodeling pathway, and the chromatin remodeling pathway (3)(4)(5)(6)(7)(8)(9). Despite progress in the diagnosis and treatment of HCC, its prognosis still remains unfavorable.…”

Section: Introductionmentioning

confidence: 99%

The significance of low levels of LINC RP1130-1 expression in human hepatocellular carcinoma

Xiao

Wang

Cheng³

et al. 2016

BST

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The STAT3-regulated long non-coding RNA Lethe promote the HCV replication

Cited by 24 publications

References 24 publications

Long non-coding RNAs (lncRNAs) and their transcriptional control of inflammatory responses

Long non-coding RNAs (lncRNAs) and their transcriptional control of inflammatory responses

Long non‐coding RNA: a versatile regulator of the nuclear factor‐κB signalling circuit

The significance of low levels of LINC RP1130-1 expression in human hepatocellular carcinoma

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