Analysis of long noncoding RNA expression in hepatocellular carcinoma of different viral etiology

Zhang, Quan; Matsuura, Kiyotaka; Kleiner, David E.; Zamboni, Fausto; Alter, Harvey J.; Farci, Patrizia

doi:10.1186/s12967-016-1085-4

Cited by 60 publications

(55 citation statements)

References 51 publications

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“…Because HULC can influence lipid biosynthesis in liver, we probed the level of HULC during HCV infection. The results were found to be in the expected line with earlier reports including patient samples (Hammerle, Gutschner, et al, ; Zhang et al, ; Zhang et al, ). So we further investigated the relevance of HULC in hepatitis C virus life cycle and its ensued pathogenesis.…”

Section: Introductionsupporting

confidence: 91%

lncRNA HULC facilitates efficient loading of HCV‐core protein onto lipid droplets and subsequent virus‐particle release

Sharma

Tripathi

2019

Cellular Microbiology

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The cellular lipid pool plays a central role in hepatitis C virus (HCV) life cycle, from establishing infection to virus propagation. Here, we show that a liver abundant long noncoding RNA, highly upregulated in liver carcinoma (HULC), is upregulated during HCV infection and manipulates the lipid pool to favour virus life cycle. Interestingly, HULC was found to be crucial for the increase in number of lipid droplets in infected cells. This effect was attributed to the role of HULC in lipid biogenesis. Further, we demonstrated that HULC knockdown decreases the association of HCV-core protein with lipid droplets. This exhibited a direct consequence on the release of HCV particles. The role of HULC in HCV-particle release was further substantiated by additional knockdown and mutation experiments. Additionally, we found that increased level of HULC in HCV-infected cells was a result of Retinoid X Receptor Alpha (RXRA)-mediated transcription, which seemed to be aided by HCV-core protein.Taken together, the results identify a distinct role of long noncoding RNA HULC in lipid dynamics during HCV infection, which provides new insights into the complex process of HCV propagation and pathogenesis.

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Section: Introductionsupporting

confidence: 91%

lncRNA HULC facilitates efficient loading of HCV‐core protein onto lipid droplets and subsequent virus‐particle release

Sharma

Tripathi

2019

Cellular Microbiology

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“…Although many attributes of LncRNAs, such as patterns of expression, remain largely unknown, LncRNAs have been shown to play important roles in transcriptional, posttranscriptional, translational and epigenetic gene regulation [9,10]. An increasing amount of evidence has revealed that different LncRNAs might be associated with HCC [11]. With regard to these latter effects, previous molecular-based studies found that certain LncRNAs promote tumor initiation, cancer cell growth, and metastasis during the development of HCC [12][13][14].…”

Section: Introductionmentioning

confidence: 99%

Long Noncoding RNA HOST2 Promotes Epithelial-Mesenchymal Transition, Proliferation, Invasion and Migration of Hepatocellular Carcinoma Cells by Activating the JAK2-STAT3 Signaling Pathway

Tan

Wang

et al. 2018

Cell Physiol Biochem

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Background/Aims: This study aims to examine the effect of long noncoding RNA HOST2 (LncRNA HOST2) on epithelial-mesenchymal transition (EMT), proliferation, invasion and migration of hepatocellular carcinoma (HCC) cells via activation of the JAK2-STAT3 signaling pathway. Methods: HCC and para-cancerous tissues were collected from 136 HCC patients. Immunohistochemistry was used to detect the expression of JAK2 and STAT3. HCC SMMC7721 cells were grouped into blank, negative control (NC), HOST2 mimic and HOST2 inhibitor groups. The mRNA and protein expression levels of HOST2, JAK2, STAT3, E-cadherin, vimentin, Snail, Slug, Twist and Zeb1 in tissues and cells were determined by reverse transcription -quantitative polymerase chain reaction (RT-qPCR) and Western blotting, respectively. An MTT assay, scratch test and Transwell assay were applied to measure cell proliferation, migration and invasion, respectively. Results: The levels of JAK2, STAT3 and vimentin were higher in HCC tissues, while the expression of E-cadherin was lower in HCC tissues compared with para-cancerous tissues. The silencing of HOST2 significantly decreased cell proliferation, migration and invasion, reduced the levels of HOST2, JAK2, STAT3 and vimentin, and elevated the expression of E-cadherin. HOST2 silencing also decreased the levels of Snail, Slug and Twist but increased the level of Zeb1 protein, while the opposite findings were observed in the HOST2 mimic group. Conclusion: These results reveal a possible mechanism in HCC in which LncRNA HOST2 may increase EMT and enhance proliferation, invasion and metastasis of HCC cells via activation of the JAK2-STAT3 signaling pathway.

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“…The development of effective treatment is critical for ischemia stroke, because it causes high mortality and disability worldwide. LncRNAs are a newly discovered class of regulators in the cerebral vascular endothelium after ischemic injury, such as stroke [29]. In recent years, non-coding RNAs have emerged as novel targets to treat ischemia stroke [30,31].…”

Section: Discussionmentioning

confidence: 99%

LncRNA MALAT1 silencing protects against cerebral ischemia-reperfusion injury through miR-145 to regulate AQP4

et al. 2020

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Background: The present study aimed to verify whether long noncoding RNA (lncRNA) MALAT1 is involved in brain tissue damage induced by ischemia-reperfusion injury, and to explore the mechanism by which MALAT1 regulates aquaporin 4 (AQP4). Methods: In this study, we established glucose deprivation (OGD)/reoxygenation (RX) astrocyte cell model and middle cerebral artery occlusion (MCAO)/reperfusion mouse model in vitro and in vivo. Then cell counting kit-8 assay, flow cytometry analysis, Triphenyltetrazolium chloride (TTC) staining, and western blotting were used to determine cell viability, cell apoptosis, cerebral infarction volume, and the abundance of AQP4, respectively. Results:We found that the level of MALAT1 was significantly upregulated in both the MCAO/reperfusion model and OGD/RX model. Knockdown of MALAT1 increased cell viability and reduced cell apoptosis in MA-C cells, while an AQP4 siRNA combined with a siRNA targeting MALAT1 could not enhance this effect. Further experiments showed that MALAT1 positively regulated AQP4 expression via miR-145. The MALAT1 siRNA did not alleviate the exacerbation of damage after miR-145 inhibitor action. However, an miR-145 inhibitor reversed the protection effects of MALAT1, indicating that MALAT1 silencing protects against cerebral ischemia-reperfusion injury through miR-145. TTC staining showed that the infracted area of whole brain was significantly attenuated in treated with sh-MALAT1 group in vivo. Conclusion:Taken together, our study confirmed that MALAT1 promotes cerebral ischemia-reperfusion injury by affecting AQP4 expression through competitively binding miR-145, indicating that MALAT1 might be a new therapeutic target for treatment cerebral ischemic stroke.

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Analysis of long noncoding RNA expression in hepatocellular carcinoma of different viral etiology

Cited by 60 publications

References 51 publications

lncRNA HULC facilitates efficient loading of HCV‐core protein onto lipid droplets and subsequent virus‐particle release

lncRNA HULC facilitates efficient loading of HCV‐core protein onto lipid droplets and subsequent virus‐particle release

Long Noncoding RNA HOST2 Promotes Epithelial-Mesenchymal Transition, Proliferation, Invasion and Migration of Hepatocellular Carcinoma Cells by Activating the JAK2-STAT3 Signaling Pathway

LncRNA MALAT1 silencing protects against cerebral ischemia-reperfusion injury through miR-145 to regulate AQP4

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