Long noncoding RNA XIST enhances ethanol‐induced hepatic stellate cells autophagy and activation via miR‐29b/HMGB1 axis

Xie, Zhengyuan; Wang, Fenfen; Xing, Zhihua; Liu, Si-Fu; Lai, Yue-Liang; Tang, S

doi:10.1002/iub.2140

Cited by 29 publications

(26 citation statements)

References 23 publications

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“…A recent study demonstrated that XIST was upregulated in ethanol-induced human hepatic stellate cells and contributed toward liver fibrogenesis (20), which was consistent with the results of the present study. Furthermore, the results of the present study suggested that XIST-overexpression promoted proliferation and enhanced the protein expression of fibrosis-related proteins in HCFs, while XIST-silencing had the opposite effect.…”

Section: Discussionsupporting

confidence: 93%

Long non‑coding RNA XIST promotes the proliferation of cardiac fibroblasts and the accumulation of extracellular matrix by sponging microRNA‑155‑5p

Zhang

Liu

et al. 2021

Exp Ther Med

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Acute myocardial infarction (AMI) is characterized by cardiomyocyte death followed by myocardial fibrosis, eventually leading to heart failure. Long non-coding (lnc)RNA X-inactive specific transcript (XIST) serves a vital role in the regulation of fibrosis. The aim of the present study was to determine whether myocardial fibrosis may be regulated by XIST and to elucidate the underlying mechanism. The relative mRNA expression levels of the target genes were evaluated using reverse transcription-quantitative polymerase chain reaction. Cell viability and apoptosis were determined using a Cell Counting Kit-8 assay and flow cytometry, respectively. The apoptosis and fibrosis-related protein expression levels were detected using western blot analysis. Finally, the interaction between XIST and microRNA (miR)-155-5p was analyzed using a luciferase reporter assay. XIST-overexpression increased proliferation and the expression level of the fibrosis-related proteins in the human cardiac fibroblast cells (HCFs). XIST directly targeted miR-155-5p and downregulated its expression, while miR-155-5p downregulation abolished the effect of XIST-silencing on cell viability and the expression level of the fibrosis-related proteins in the HCFs. XIST promoted cell proliferation and the expression level of fibrosis-related proteins by sponging miR-155-5p. Therefore, XIST may represent a novel effective target for AMI treatment.

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Section: Discussionsupporting

confidence: 93%

Long non‑coding RNA XIST promotes the proliferation of cardiac fibroblasts and the accumulation of extracellular matrix by sponging microRNA‑155‑5p

Zhang

Liu

et al. 2021

Exp Ther Med

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“…In hypoxic‐induced H9c2 cells, miR‐29b has been proposed to regulate autophagic activity by directly targeting secreted protein acidic and rich in cysteine gene (Zhou et al, 2019). In hepatic stellate cells, two different genes, Atg9a and high‐mobility group box‐1 (HMGB1) have been found to be responsible for regulatory effect on autophagy upon different stimuli (Kong et al, 2019; Xie et al, 2019). In the context of glioma, upregulation of miR‐29b has been shown to be correlated with increased level of autophagy (Kim et al, 2019).…”

Section: Discussionmentioning

confidence: 99%

Micro‐RNA29b enhances the sensitivity of glioblastoma multiforme cells to temozolomide by promoting autophagy

Yang

Zhang

et al. 2020

The Anatomical Record

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To explore whether or not aberrant expression of miR‐29b in glioblastoma multiforme (GBM) cells was associated with temozolomide (TMZ) resistance and to elucidate potential underlying mechanisms. Upregulation of miR‐29 in GBM cells was achieved by transfecting miR‐29b mimics. Changes in cell viability were measured by using CCK‐8 assays. Flow cytometry and TUNEL assays were used to quantify the number of apoptotic cells. The expression levels of apoptosis‐related proteins as well as autophagy‐associated proteins, and the expression levels of both apoptotic and autophagic genes were determined by Western blotting. Autophagy flux was monitored by transfecting mRFP‐GFP‐LC3 adenovirus. We halted autophagy by introducing Atg 5‐specific siRNA or the autophagy inhibitor Bafilomycin A1 (Baf‐A1). We also employed a GBM xenograft mice model to confirm the role of miR‐29b in vivo. miR‐29b overexpression induced inhibition of cell viability, and also induced apoptosis and autophagy in U251 and U87MG cells. Furthermore, upregulation of miR‐29b was able to potentiate the level of antitumor activity of TMZ against tested cells. We also found that autophagy induced by miR‐29b, at least partially, contributed to the increase of TMZ sensitivity in GBM cells. As was evidenced by blockade of autophagy, the application of Atg 5 siRNA or Baf‐A1 was able to significantly reverse these effects. Consistent with observations in vitro, findings of in vivo assessment also confirmed that overexpression of miR‐29b was able to effectively halt tumor growth and enhance the antitumor activity of TMZ. miR‐29b potentiates TMZ sensitivity against GBM cells by inducing autophagy and the combined use of miR‐29 mimic and TMZ might represent a potential therapeutic strategy for GBM patients.

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“…As with other lncRNAs, lncRNA XIST functioned as a competitive endogenous RNA (ceRNA) and harbored putative binding sites of miR-29b, which directly targeted and inhibited the expression of HMGB1. Hence, lncRNA XIST upregulated HMGB1 expression, promoted ethanol-induced autophagy and eventually activated HSCs 37 . G protein-coupled receptors (GPCRs) play complex roles in cellular signal transduction in HSC activation.…”

Section: Liver Fibrosis and Autophagymentioning

confidence: 98%

Self-eating: friend or foe? The emerging role of autophagy in fibrotic diseases

Liu¹,

Wu²,

Li³

2020

Theranostics

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Fibrosis occurs in most human organs including the liver, lung, heart and kidney, and is crucial for the progression of most chronic diseases. As an indispensable catabolic process for intracellular quality control and homeostasis, autophagy occurs in most mammalian cells and is implicated in many biological processes including fibrogenesis. Although advances have been made in understanding autophagy process, the potential role of autophagy in fibrotic diseases remains controversial and has recently attracted a great deal of attention. In the current review, we summarize the commonalities of autophagy affecting different types of fibrosis in different organs, including the liver, lung, heart, and kidney as well as in cystic fibrosis, systematically outline the contradictory results and highlight the distinct role of autophagy during the various stages of fibrosis. In summary, the exact role autophagy plays in fibrogenesis depends on specific cell types and different stimuli, and identifying and evaluating the pathogenic contribution of autophagy in fibrogenesis will promote the discovery of novel therapeutic strategies for the clinical management of these fibrotic diseases.

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Long noncoding RNA XIST enhances ethanol‐induced hepatic stellate cells autophagy and activation via miR‐29b/HMGB1 axis

Cited by 29 publications

References 23 publications

Long non‑coding RNA XIST promotes the proliferation of cardiac fibroblasts and the accumulation of extracellular matrix by sponging microRNA‑155‑5p

Long non‑coding RNA XIST promotes the proliferation of cardiac fibroblasts and the accumulation of extracellular matrix by sponging microRNA‑155‑5p

Micro‐RNA29b enhances the sensitivity of glioblastoma multiforme cells to temozolomide by promoting autophagy

Self-eating: friend or foe? The emerging role of autophagy in fibrotic diseases

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