The lncRNA H19 alleviates muscular dystrophy by stabilizing dystrophin

Zhang, Yaohua; Li, Yajuan; Hu, Qingsong; Xi, Yutao; Xing, Zhen; Zhang, Zhao; Huang, Li; Wu, Jianbo; Liang, Ke; Nguyen, Tina K.; Egranov, Sergey D.; Sun, Chengcao; Zhao, Zilong; Hawke, David H.; Li, Jin; Sun, Deqiang; Kim, Jean J.; Zhang, Ping; Cheng, Jie; Abid, Farida; Hung, Mien‐Chie; Han, Leng; Darabi, Radbod; Lin, Chunru; Yang, Liuqing

doi:10.1038/s41556-020-00595-5

Cited by 60 publications

(48 citation statements)

References 63 publications

(48 reference statements)

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“…Among these non-coding RNAs, microRNAs have been sufficiently demonstrated by us and others to exert critical regulatory roles in various cancers (Yuan et al, 2011;Chang et al, 2014Chang et al, , 2017. Long non-coding RNAs (lncRNAs) are another class of noncoding RNAs with more than 200 nucleotides in length (Ponting et al, 2009;Zhang Y. et al, 2020). lncRNAs have been gradually revealed to exhibit regulatory roles in a variety of cancers (Schmitt and Chang, 2016).…”

Section: Introductionmentioning

confidence: 99%

ITGB1-DT Facilitates Lung Adenocarcinoma Progression via Forming a Positive Feedback Loop With ITGB1/Wnt/β-Catenin/MYC

Chang

Xiao

et al. 2021

Front. Cell Dev. Biol.

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Lung adenocarcinoma (LUAD) is the main histological type of lung cancer, which is the leading cause of cancer-related deaths. Long non-coding RNAs (lncRNAs) were recently revealed to be involved in various cancers. However, the clinical relevance and potential biological roles of most lncRNAs in LUAD remain unclear. Here, we identified a prognosis-related lncRNA ITGB1-DT in LUAD. ITGB1-DT was upregulated in LUAD and high expression of ITGB1-DT was correlated with advanced clinical stages and poor overall survival and disease-free survival. Enhanced expression of ITGB1-DT facilitated LUAD cellular proliferation, migration, and invasion, and also lung metastasis in vivo. Knockdown of ITGB1-DT repressed LUAD cellular proliferation, migration, and invasion. ITGB1-DT interacted with EZH2, repressed the binding of EZH2 to ITGB1 promoter, reduced H3K27me3 levels at ITGB1 promoter region, and therefore activated ITGB1 expression. Through upregulating ITGB1, ITGB1-DT activated Wnt/β-catenin pathway and its downstream target MYC in LUAD. The expressions of ITGB1-DT, ITGB1, and MYC were positively correlated with each other in LUAD tissues. Intriguingly, ITGB1-DT was found as a transcriptional target of MYC. MYC directly transcriptionally activated ITGB1-DT expression. Thus, ITGB1-DT formed a positive feedback loop with ITGB1/Wnt/β-catenin/MYC. The oncogenic roles of ITGB1-DT were reversed by depletion of ITGB1 or inhibition of Wnt/β-catenin pathway. In summary, these findings revealed ITGB1-DT as a prognosis-related and oncogenic lncRNA in LUAD via activating the ITGB1-DT/ITGB1/Wnt/β-catenin/MYC positive feedback loop. These results implicated ITGB1-DT as a potential prognostic biomarker and therapeutic target for LUAD.

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Section: Introductionmentioning

confidence: 99%

ITGB1-DT Facilitates Lung Adenocarcinoma Progression via Forming a Positive Feedback Loop With ITGB1/Wnt/β-Catenin/MYC

Chang

Xiao

et al. 2021

Front. Cell Dev. Biol.

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“…Results from studies using different cell types support that H19 is mainly, even exclusively, expressed in the cytoplasm 43 – 45 . Based on this subcellular location, competing endogenous RNA regulation is the most reported mechanism of action of H19, followed by direct binding to transcription regulators or other proteins 46 , 47 . Currently, few study have investigated the role of H19 in regulating mRNA translation.…”

Section: Discussionmentioning

confidence: 99%

LncRNA H19 governs mitophagy and restores mitochondrial respiration in the heart through Pink1/Parkin signaling during obesity

et al. 2021

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Maintaining proper mitochondrial respiratory function is crucial for alleviating cardiac metabolic disorders during obesity, and mitophagy is critically involved in this process. Long non-coding RNA H19 (H19) is crucial for metabolic regulation, but its roles in cardiac disorders, mitochondrial respiratory function, and mitophagy during obesity are largely unknown. In this study, palmitic acid (PA)-treated H9c2 cell and Lep−/− mice were used to investigate cardiac metabolic disorders in vitro and in vivo, respectively. The effects of H19 on metabolic disorders, mitochondrial respiratory function, and mitophagy were investigated. Moreover, the regulatory mechanisms of PA, H19, mitophagy, and respiratory function were examined. The models tested displayed a reduction in H19 expression, respiratory function and mitochondrial number and volume, while the expression of mitophagy- and Pink1/Parkin signaling-related proteins was upregulated, as indicated using quantitative real-time PCR, Seahorse mitochondrial stress test analyzer, transmission electron microscopy, fluorescence indicators and western blotting. Forced expression of H19 helped to the recoveries of respiratory capacity and mitochondrial number while inhibited the levels of mitophagy- and Pink1/Parkin signaling-related proteins. Pink1 knockdown also attenuated PA-induced mitophagy and increased respiratory capacity. Mechanistically, RNA pull-down, mass spectrometry, and RNA-binding protein immunoprecipitation assays showed that H19 could hinder the binding of eukaryotic translation initiation factor 4A, isoform 2 (eIF4A2) with Pink1 mRNA, thus inhibiting the translation of Pink1 and attenuation of mitophagy. PA significantly increased the methylation levels of the H19 promoter region by upregulation Dnmt3b methylase levels, thereby inhibiting H19 transcription. Collectively, these findings suggest that DNA methylation-mediated the downregulation of H19 expression plays a crucial role in cardiomyocyte or H9c2 cells metabolic disorders and induces cardiac respiratory dysfunction by promoting mitophagy. H19 inhibits excessive mitophagy by limiting Pink1 mRNA translation, thus alleviating this cardiac defect that occurs during obesity.

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“…H19 was also shown to play an important role in various cardiovascular diseases such as acute myocardial infarction (Huang et al 2020 ), myocardial I/RI (Li et al 2019a , b ) and cardiomyocyte hypertrophy (Viereck et al 2020 ). It has also been confirmed that H19 plays a noticeable role in embryonic placental growth, skeletal muscle differentiation and related diseases (Dey et al 2014 ; Zhang et al 2020 ).…”

Section: Introductionmentioning

confidence: 88%

The role and mechanism of long non-coding RNA H19 in stem cell osteogenic differentiation

Wang

2021

Mol Med

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Background In recent years, H19, as one of the most well-known long non-coding RNA, has been reported to play important roles in many biological and physiological processes. H19 has been identified to regulate the osteogenic differentiation of various stem cells in many studies. However, the detailed role and regulation mechanism of H19 was not consistent in the reported studies. Main body of the manuscript In this review article we summarized the effect and mechanism of lncRNA H19 on osteogenic differentiation of various stem cells reported in the published literatures. The role and mechanism of H19, H19 expression changes, effect of H19 on cell proliferation in osteogenic differentiation were respectively reviewed. Conclusions An increasing number of studies have provided evidence that H19 play its role in the regulation of stem cell osteogenic differentiation by different mechanisms. Most of the studies favored the positive regulatory effect of H19 through lncRNA-miRNA pathway. The function and underlying mechanisms by which H19 contributes to osteogenic differentiation require further investigation.

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The lncRNA H19 alleviates muscular dystrophy by stabilizing dystrophin

Cited by 60 publications

References 63 publications

ITGB1-DT Facilitates Lung Adenocarcinoma Progression via Forming a Positive Feedback Loop With ITGB1/Wnt/β-Catenin/MYC

ITGB1-DT Facilitates Lung Adenocarcinoma Progression via Forming a Positive Feedback Loop With ITGB1/Wnt/β-Catenin/MYC

LncRNA H19 governs mitophagy and restores mitochondrial respiration in the heart through Pink1/Parkin signaling during obesity

The role and mechanism of long non-coding RNA H19 in stem cell osteogenic differentiation

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