A long non-coding RNA,<i>APOA4</i>-AS, regulates<i>APOA4</i>expression depending on HuR in mice

Qin, Weiping; Li, Xinzhi; Xie, Liwei; Li, Sha; Liu, Jianan; Jia, Linna; Dong, Xue; Ren, Xiaomeng; Xiao, Junjie; Yang, Changqing; Zhou, Yifa; Chen, Zheng

doi:10.1093/nar/gkw341

Cited by 66 publications

(53 citation statements)

References 44 publications

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“…Apoa4 is a critical gene involved in the regulation of multiple metabolic pathways, including lipid absorption, lipid metabolism, and glucose homeostasis . Emerging evidence suggests a critical role of apolipoproteins, including APOA4, in the pathogenesis of NAFLD Specifically, Kang et al demonstrated that over‐expression of APOA4 promotes lipid accumulation in the liver, and Qin et al reported that the level of APOA4 protein was increased in the genetically obese ( ob/ob ) mice. Furthermore, a marked upregulation of APOA4, as well as SERPINE1 and IGFBP1, has been demonstrated in patients with NAFLD.…”

Section: Discussionmentioning

confidence: 99%

Identification of chromatin‐accessible domains in non‐alcoholic steatohepatitis‐derived hepatocellular carcinoma

Dechassa

Tryndyak

Conti

et al. 2018

Molecular Carcinogenesis

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Non-alcoholic steatohepatitis (NASH) is becoming one of the major causes of hepatocellular carcinoma (HCC) in the United States and Western countries; however, the molecular mechanisms associated with NASH-related liver carcinogenesis are not well understood. In the present study, we investigated cancer-associated chromatin alterations using a model that resembles the development of NASH-related HCC in humans. An assay for transposase-accessible chromatin with high throughput sequencing (ATAC-seq) identified 1677 tumor-specific chromatin-accessible regions in NASH-derived HCC tissue samples. Using a combined analysis of ATAC-seq and global gene expression data, we identified 199 differentially expressed genes, 139 up-regulated and 60 down-regulated. Interestingly, 15 of the 139 up-regulated genes had accessible chromatin sites within 5 Kb of the transcription start site (TSS), including Apoa4, Anxa2, Serpine1, Igfbp1, and Tubb2a, genes critically involved in the development of NASH and HCC. We demonstrate that the mechanism for the up-regulation of these genes is associated with the enrichment of chromatin-accessible regions by transcription factors, especially NFATC2, and histone H3K4me1 and H3K27ac gene transcription-activating marks. These data underline the important role of chromatin accessibility perturbations in reshaping of the chromatin landscape in NASH-related HCC.

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Section: Discussionmentioning

confidence: 99%

Identification of chromatin‐accessible domains in non‐alcoholic steatohepatitis‐derived hepatocellular carcinoma

Dechassa

Tryndyak

Conti

et al. 2018

Molecular Carcinogenesis

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show abstract

“…HEK293 and Hepa1 cells were grown at 37°C in 5% CO 2 in DMEM supplemented with 100 U/ml penicillin, 100 U/ml streptomycin, and 10% fetal bovine serum. Primary hepatocytes were isolated from C57BL/6 WT mice (16, 17). Hepa1 cells and primary hepatocytes were then infected with adenoviruses (8, 18).…”

Section: Methodsmentioning

confidence: 99%

“…Total RNAs were extracted using TriPure Isolation Reagent (Roche Diagnostics, Mannheim, Germany), and the first‐strand cDNAs were synthesized with random primers and M‐MLV reverse transcriptase (Promega) (16). RNA abundance was measured with qPCR SYBR Mix and a LightCycler 480 real‐time PCR system (both from Roche Diagnostics).…”

Section: Methodsmentioning

confidence: 99%

A small‐molecule inhibitor of NF‐κB‐inducing kinase (NIK) protects liver from toxin‐induced inflammation, oxidative stress, and injury

Ren

Jia

et al. 2016

FASEB j.

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Potent and selective chemical probes are valuable tools for discovery of novel treatments for human diseases. NF-κB-inducing kinase (NIK) is a key trigger in the development of liver injury and fibrosis. Whether inhibition of NIK activity by chemical probes ameliorates liver inflammation and injury is largely unknown. In this study, a small-molecule inhibitor of NIK, B022, was found to be a potent and selective chemical probe for liver inflammation and injury. B022 inhibited the NIK signaling pathway, including NIK-induced p100-to-p52 processing and inflammatory gene expression, both in vitro and in vivo Furthermore, in vivo administration of B022 protected against not only NIK but also CCl-induced liver inflammation and injury. Our data suggest that inhibition of NIK is a novel strategy for treatment of liver inflammation, oxidative stress, and injury.-Ren, X., Li, X., Jia, L., Chen, D., Hou, H., Rui, L., Zhao, Y., Chen, Z. A small-molecule inhibitor of NF-κB-inducing kinase (NIK) protects liver from toxin-induced inflammation, oxidative stress, and injury.

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“…The mechanisms by which lncRNAs function are highly dependent on their subcellular location . Cytoplasmic lncRNAs often act as crucial regulators by binding specific proteins . We therefore aimed to identify CAAlnc1‐interacting proteins using a biotinylated‐CAAlnc1 pull‐down assay.…”

Section: Resultsmentioning

confidence: 99%

Cachexia‐related long noncoding RNA, CAAlnc1, suppresses adipogenesis by blocking the binding of HuR to adipogenic transcription factor mRNAs

Shen

Han

et al. 2019

Intl Journal of Cancer

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Cancer‐associated cachexia (CAC) is a devastating syndrome characterized by progressive losses of adipose tissue and skeletal muscle. CAC‐related adipose tissue loss (CAL) occurs early and is associated with a shorter survival time. To explore potential regulatory long noncoding RNAs (lncRNAs) of CAL, RNA microarrays were used to analyze the transcriptomes of white adipose tissue from CAC mice vs. control mice. A set of differentially expressed lncRNAs was identified, and among them was CAAlnc1, which suppressed adipogenesis of C3H10 cells as demonstrated by gain‐of‐function and loss‐of‐function experiments. RNA immunoprecipitation and pull‐down assays revealed Hu antigen R (HuR) was an important binding partner of CAAlnc1. The interaction between CAAlnc1 and HuR blocked the binding of HuR to adipogenic transcription factor mRNAs and further downregulated the expression of these transcription factors. This study generated a list of CAL‐related lncRNAs and provided details of a functional lncRNA which may play an important role in CAL.

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A long non-coding RNA,APOA4-AS, regulatesAPOA4expression depending on HuR in mice

Cited by 66 publications

References 44 publications

Identification of chromatin‐accessible domains in non‐alcoholic steatohepatitis‐derived hepatocellular carcinoma

Identification of chromatin‐accessible domains in non‐alcoholic steatohepatitis‐derived hepatocellular carcinoma

A small‐molecule inhibitor of NF‐κB‐inducing kinase (NIK) protects liver from toxin‐induced inflammation, oxidative stress, and injury

Cachexia‐related long noncoding RNA, CAAlnc1, suppresses adipogenesis by blocking the binding of HuR to adipogenic transcription factor mRNAs

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