Long noncoding RNA in liver diseases

Takahashi, Kenji; Yan, Irene K.; Haga, Hiroaki; Patel, Tushar

doi:10.1002/hep.27043

Cited by 174 publications

(154 citation statements)

References 54 publications

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“…Therefore, better understanding of the molecular mechanisms involved in HCC invasion and metastasis is essential for the improvement of diagnosis, therapy and prognosis prediction of HCC. Recently, accumulating evidence indicate that long noncoding RNAs (lncRNAs) play a crucial role in HCC pathogenesis, providing new insights into the biology of this disease [5].…”

Section: Introductionmentioning

confidence: 99%

Upregulation of Long Non-Coding RNA PlncRNA-1 Promotes Metastasis and Induces Epithelial-Mesenchymal Transition in Hepatocellular Carcinoma

Dong

Ni²,

Hu³

et al. 2016

Cell Physiol Biochem

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Background/Aims: PlncRNA-1 has been demonstrated to promote malignancy in various cancers. The present study aims to investigate the expression pattern, prognosis value and the function of PlncRNA-1 in human hepatocellular carcinoma (HCC). Methods: The expression of PlncRNA-1 in 84 pairs of HCC and their matched normal tissues was examined by quantitative real-time polymerase chain reaction (qRT-PCR). The correlations of PlncRNA-1 expression and clinicopathological characteristics and prognosis were also analyzed. The biological role of PlncRNA-1 in cell proliferation, migration and invasion was examined in vitro and in vivo. Results: The results showed that the level of PlncRNA-1 expression was significantly increased in HCC tissues and significantly correlated with tumor size, vascular invasion and advanced TNM stage. Moreover, patients with high levels of PlncRNA-1 expression had relatively poor prognostic outcomes, serving as an independent prognostic factor for HCC. In vitro functional assays indicated that knockdown of PlncRNA-1 expression significantly reduced cell proliferation, migration and invasion by inhibiting the epithelial-mesenchymal transition (EMT) signaling. Animal model experiments confirmed the ability of PlncRNA-1 to promote tumor growth in vivo. Conclusions: Taken together, our findings suggest that PlncRNA-1 may serve as an oncogene in HCC progression and represent a valuable prognostic marker and potential therapeutic target for HCC.

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Section: Introductionmentioning

confidence: 99%

Upregulation of Long Non-Coding RNA PlncRNA-1 Promotes Metastasis and Induces Epithelial-Mesenchymal Transition in Hepatocellular Carcinoma

Dong

Ni²,

Hu³

et al. 2016

Cell Physiol Biochem

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“…Several lincRNAs, including H19 (64,65), Meg3 (27,66), and HULC (26,67), have been associated with diseases showing a significant sex-biased prevalence in humans, notably hepatocellular carcinoma and liver fibrosis, and liver regeneration (68,69). However, it is unknown whether these or other lincRNAs are expressed in a sex-dependent manner in liver, where they might be subject to tight regulation by GH and have the potential to contribute to the widespread sex differences that characterize liver function and disease susceptibility.…”

mentioning

confidence: 99%

Hepatic Long Intergenic Noncoding RNAs: High Promoter Conservation and Dynamic, Sex-Dependent Transcriptional Regulation by Growth Hormone

Melia

Hao

Yilmaz

et al. 2016

Molecular and Cellular Biology

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Long intergenic noncoding RNAs (lincRNAs) are increasingly recognized as key chromatin regulators, yet few studies have characterized lincRNAs in a single tissue under diverse conditions. Here, we analyzed 45 mouse liver RNA sequencing (RNA-Seq) data sets collected under diverse conditions to systematically characterize 4,961 liver lincRNAs, 59% of them novel, with regard to gene structures, species conservation, chromatin accessibility, transcription factor binding, and epigenetic states. To investigate the potential for functionality, we focused on the responses of the liver lincRNAs to growth hormone stimulation, which imparts clinically relevant sex differences to hepatic metabolism and liver disease susceptibility. Sex-biased expression characterized 247 liver lincRNAs, with many being nuclear RNA enriched and regulated by growth hormone. The sex-biased lincRNA genes are enriched for nearby and correspondingly sex-biased accessible chromatin regions, as well as sex-biased binding sites for growth hormone-regulated transcriptional activators (STAT5, hepatocyte nuclear factor 6 [HNF6], FOXA1, and FOXA2) and transcriptional repressors (CUX2 and BCL6). Repression of female-specific lincRNAs in male liver, but not that of male-specific lincRNAs in female liver, was associated with enrichment of H3K27me3-associated inactive states and poised (bivalent) enhancer states. Strikingly, we found that liver-specific lincRNA gene promoters are more highly species conserved and have a significantly higher frequency of proximal binding by liver transcription factors than liver-specific protein-coding gene promoters. Orthologs for many liver lincRNAs were identified in one or more supraprimates, including two rat lincRNAs showing the same growth hormone-regulated, sex-biased expression as their mouse counterparts. This integrative analysis of liver lincRNA chromatin states, transcription factor occupancy, and growth hormone regulation provides novel insights into the expression of sexspecific lincRNAs and their potential for regulation of sex differences in liver physiology and disease. High-throughput sequencing of mammalian transcriptomes has revealed nearly ubiquitous transcription of the genome and the generation of large numbers of noncoding transcripts. Noncoding RNAs (ncRNAs) have drawn much attention as potential chromatin regulators, exemplified by classical ncRNAs, such as Xist (1). Several thousand ncRNAs have been discovered in human (2, 3), mouse (4-7), zebrafish (8,9), and fruit fly (10,11). Individual ncRNAs were shown to play diverse regulatory roles in gene expression (9,(12)(13)(14)(15); however, the vast majority of ncRNAs are poorly characterized, both computationally and experimentally. Many ncRNAs share salient features of protein-coding genes, including transcription by RNA polymerase II, 5= capping, splicing, polyadenylation, and deposition of histone marks associated with transcription, specifically H3K4me3 at the promoter and H3K36me3 across the gene body (4). These ncRNAs are typically Ͼ200 nucleo...

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“…lncRNAs play crucial roles in multiple developmental processes and diseases at almost every gene expression regulation level [24,25,26,27]. Antisense RNAs usually regulate their counterpart sense mRNA in cis by bridging epigenetic effectors and regulatory complexes at specific genomic loci [28].…”

Section: Discussionmentioning

confidence: 99%

Distinct Expression Profiles of lncRNAs Between Regressive and Mature Scars

Long

et al. 2015

Cell Physiol Biochem

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Background: Recent studies suggest that long non-coding RNAs (lncRNAs) play crucial roles in human diseases. The function of lncRNAs in abnormal scar pathogenesis remains poorly understood. Methods: In this study, we examined the lncRNAs expression profiles among regressive and mature scars following caesarean sections. A total of 30,586 lncRNAs and 26,109 mRNAs were analyzed by microarrays (Human LncRNA Array v3.0, Arraystar, Inc.). Results: In total, we identified 1,871 lncRNAs and 817 mRNAs with differential expression between regressive and mature scar individuals (fold change≥3, p≤0.001). A set of differentially expressed lncRNA transcripts, in particular, lncRNA8975-1, AC097662.2 and RP11-586K2.1, were confirmed using qRT-PCR. Gene ontology and pathway analysis revealed that compared to mature scars, many processes over-represented in regressive scars are related to the immune system. Conclusion: Our results show significantly altered expression profiles of lncRNAs and mRNAs between regressive and mature scars. These transcripts are potential molecular targets for inhibiting abnormal scar formation following caesarean sections.

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Long noncoding RNA in liver diseases

Cited by 174 publications

References 54 publications

Upregulation of Long Non-Coding RNA PlncRNA-1 Promotes Metastasis and Induces Epithelial-Mesenchymal Transition in Hepatocellular Carcinoma

Upregulation of Long Non-Coding RNA PlncRNA-1 Promotes Metastasis and Induces Epithelial-Mesenchymal Transition in Hepatocellular Carcinoma

Hepatic Long Intergenic Noncoding RNAs: High Promoter Conservation and Dynamic, Sex-Dependent Transcriptional Regulation by Growth Hormone

Distinct Expression Profiles of lncRNAs Between Regressive and Mature Scars

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