Overexpression of micro<scp>RNA</scp>‐30a inhibits hepatitis B virus X protein‐induced autophagosome formation in hepatic cells

Kumar, Sunil; Gupta, Parul; Khanal, Sweta; Shahi, Aashirwad; Kumar, Pushpendra; Sarin, Shiv Kumar; Venugopal, Senthil K.

doi:10.1111/febs.13209

Cited by 16 publications

(14 citation statements)

References 32 publications

(67 reference statements)

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“…Previous studies have shown that miRNA-30a inhibits autophagy in ischemic stroke, cardiomyopathy and some carcinomas by downregulating Beclin-1 expression (Zhu et al, 2009;Zou et al, 2012;Yin et al, 2013;Pan et al, 2013;Wang et al, 2014;Yu et al, 2012). Recently, a report by Kumar et al demonstrated that miR-30a was involved in modulating autophagosome formation induced by Hepatitis B virus X protein (HBx), and that this effect was mediated via reduced Beclin-1 expression (Kumar et al, 2015). Our data showed that miR-30a was downregulated by EV71-induced autophagy mediated by Beclin-1 and further demonstrated that Beclin-1 contains a potential binding site for miRNA-30a.…”

Section: Discussionmentioning

confidence: 99%

Enterovirus 71 induces autophagy by regulating has-miR-30a expression to promote viral replication

Chen

et al. 2015

Antiviral Research

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Enterovirus 71 (EV71), the etiological agent of hand-foot-and-mouth disease, has increasingly become a public health challenge around the world. Previous studies reported that EV71 infection can induce autophagic machinery to enhance viral replication in vitro and in vivo, but did not address the underlying mechanisms. Increasing evidence suggests that autophagy, in a virus-specific manner, may function to degrade viruses or facilitate viral replication. In this study, we reported that EV71 infection of human epidermoid carcinoma (Hep2) and African green monkey kidney cells (Vero) induced autophagy, which is beneficial for viral replication. Our investigation of the mechanisms revealed that EV71 infection resulted in the reduction of cellular miR-30a, which led to the inhibition of Beclin-1, a key autophagy-promoting gene that plays important roles at the early phase of autophagosome formation. We provided further evidence that by modulating cellular miR-30a level through either overexpression or inhibition, one can inhibit or promote EV71 replication, respectively, through regulating autophagic activity.

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Section: Discussionmentioning

confidence: 99%

Enterovirus 71 induces autophagy by regulating has-miR-30a expression to promote viral replication

Chen

et al. 2015

Antiviral Research

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“…Transfection of miR-22 premiRs, anti-miR-22 oligos or non-specific miRNA (NS) (Sigma-Aldrich, St Louis, MO, USA) was performed using siPORT™ NeoFX™ transfection reagent (Thermofisher, Carlsbad, CA, USA) as described by us previously [17]. After the experiments, the cells were collected for either total RNA isolation or protein separation.…”

Section: Methodsmentioning

confidence: 99%

Butyrate induces ROS-mediated apoptosis by modulating miR-22/SIRT-1 pathway in hepatic cancer cells

et al. 2017

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Butyrate is one of the short chain fatty acids, produced by the gut microbiota during anaerobic fermentation of dietary fibres. It has been shown that it can inhibit tumor progression via suppressing histone deacetylase and can induce apoptosis in cancer cells. However, the comprehensive pathway by which butyrate mediates apoptosis and growth arrest in cancer cells still remains unclear. In this study, the role of miR-22 in butyrate-mediated ROS release and induction of apoptosis was determined in hepatic cells. Intracellular expression of miR-22 was increased when the Huh 7 cells were incubated with sodium butyrate. Over-expression of miR-22 or addition of sodium butyrate inhibited SIRT-1 expression and enhanced the ROS production. Incubation of cells with anti-miR-22 reversed the effects of butyrate. Butyrate induced apoptosis via ROS production, cytochrome c release and activation of caspase-3, whereas addition of N-acetyl cysteine or anti-miR-22 reversed these butyrate-induced effects. Furthermore, sodium butyrate inhibited cell growth and proliferation, whereas anti-miR-22 inhibited these butyrate-mediated changes. The expression of PTEN and gsk-3 was found to be increased while p-akt and β-catenin expression was decreased significantly by butyrate. These data showed that butyrate modulated both apoptosis and proliferation via miR-22 expression in hepatic cells.

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“…The Atg family of proteins is critical for autophagy. Several of them, Atg4, Beclin‐1 and LC3, have been shown to be the targets of miRNAs such as miR‐30a and miR‐204, suggesting that miRNA can regulate autophagy. Here, we show that HBV levels are inversely correlated with the levels of cellular miRNA miR‐192‐3p in HBV patients as well as in cultured cells.…”

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confidence: 99%

Hepatitis B Virus Induces Autophagy to Promote its Replication by the Axis of miR‐192‐3p‐XIAP Through NF kappa B Signaling

et al. 2019

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Hepatitis B virus (HBV) is a major risk factor for the development and progression of hepatocellular carcinoma (HCC). It has been reported that viral infection can interfere with cellular microRNA (miRNA) expression and participate in the pathogenesis of oncogenicity. Here, we report that decreasing levels of the expression of the miRNA miR-192-3p is associated with rising levels of HBV DNA in the serum of HBV patients. We revealed that HBV infection repressed the expression of miR-192-3p through HBx interaction with c-Myc. We further showed that miR-192-3p was repressed by HBV transfection in vitro and in mouse model, leading to cellular autophagy. Using an miRNA target prediction database miRBase, we identified XIAP as a novel target gene of miR-192-3p and demonstrated that miR-192-3p directly targeted XIAP 3'-untranslated region (3'-UTR) of XIAP mRNA. Importantly, we discovered that HBV promoted autophagy through miR-192-3p-XIAP axis and that this process was important for HBV replication in vitro and in vivo. We demonstrated that miR-192-3p functioned through the NF-κB signaling pathway to inhibit autophagy, thereby reducing HBV replication. Our findings indicate that miR-192-3p is a novel regulator of HBV infection and may play a potential role in HCC. It may also serve as a new biomarker or therapeutic target for HBV patients. This article is protected by copyright. All rights reserved.

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Overexpression of microRNA‐30a inhibits hepatitis B virus X protein‐induced autophagosome formation in hepatic cells

Cited by 16 publications

References 32 publications

Enterovirus 71 induces autophagy by regulating has-miR-30a expression to promote viral replication

Enterovirus 71 induces autophagy by regulating has-miR-30a expression to promote viral replication

Butyrate induces ROS-mediated apoptosis by modulating miR-22/SIRT-1 pathway in hepatic cancer cells

Hepatitis B Virus Induces Autophagy to Promote its Replication by the Axis of miR‐192‐3p‐XIAP Through NF kappa B Signaling

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