Intrahepatic HCV RNA Level and Genotype 1 Independently Associate with Hepatic Reticulon 3 Expression

Lin, Cheng‐Jui; Chien, Rong‐Nan; Liang, Kung–Hao; Ke, Po‐Yuan; Huang, Ya‐Hui; Yeh, Chau‐Ting

doi:10.21873/anticanres.11641

Cited by 3 publications

(3 citation statements)

References 12 publications

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“…A recent report revealed increased intrahepatic RTN3 expression which correlated with higher HCV genotype 1 RNA levels [ 37 ]. Further, conflicting reports have indicated that RTN3 knockdown in cells can lead to either an increase [ 29 ] or no change [ 30 ] in intracellular HCV RNA levels.…”

Section: Resultsmentioning

confidence: 99%

“…In Flaviviruses, RNT3 was shown to be significantly enriched within membranous structural sites of virus replication [ 28 , 43 ]. In the context of HCV infection, Lin et al revealed increased intrahepatic RTN3 levels which correlated with higher HCV genotype 1 RNA levels [ 37 ]. These observations are in concert with our findings which revealed increased RTN3L&S isoforms in HCV JFH1 infected Huh7 cells and liver samples from HCV infected treatment naïve individuals.…”

Section: Discussionmentioning

confidence: 99%

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Reticulon-3 modulates the incorporation of replication competent hepatitis C virus molecules for release inside infectious exosomes

Li¹,

Abosmaha²,

Coffin³

et al. 2020

PLoS ONE

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Background Cell released microvesicles specifically, exosomes, play an important role in mediating immunologic escape, treatment resistance, and disease persistence of Hepatitis C virus (HCV) infection. Reports on the molecular compositions of exosomes released by cells under diverse conditions, especially during viral infections, suggest that their cargo contents are not randomly loaded. However, the precise molecular mechanisms directing the selective cargo sorting and loading inside infectious viral exosomes remains elusive. Aim To decipher the role of Reticulon 3 (RTN3) in the selective molecular cargo sorting and loading inside infectious viral exosomes during HCV infection. Methods We used Huh7 cells–JFH1 HCV infection and HCV Full-Length (FL) replicon systems. Additionally, we analyzed human liver and serum exosome samples from healthy and treatment naïve HCV infected individuals. Our experiments made use of molecular biology and immunology techniques. Results HCV infection (JFH1-Huh7 or HCV-FL replicon cells) was associated with increased RTN3L&S isoforms expression in cells and cell released exosomes. Accordingly, increased expression of RTN3L&S was observed in liver and serum exosome samples of HCV infected individuals compared to healthy controls. RNA-ChIP analysis revealed that RTN3L&S interacted with dsHCV RNA. Lentiviral CRISPR/Cas9 mediated knockdown (KD) of RTN3 and plasmid overexpression (OE) of wild type, C- and N-terminal deletion mutants of RTN3L&S in HCV- infected Huh7 cells differentially impacted the cellular release of infectious viral exosomes. RTN3L&S KD significantly decreased, while RTN3S OE significantly increased the number of Huh7 cell-released infectious exosomes. The C-terminal domain of RTN3 interacted with and modulated the loading of dsHCV RNA inside infectious exosomes. Antiviral treatment of HCV infected Huh7 cells reduced virus-induced RTN3L&S expression and attenuated the release of infectious exosomes. Conclusion RTN3 constitutes a novel regulator and a potential therapeutic target that mediates the specific loading of infectious viral exosomes.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Reticulon-3 modulates the incorporation of replication competent hepatitis C virus molecules for release inside infectious exosomes

Li¹,

Abosmaha²,

Coffin³

et al. 2020

PLoS ONE

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“…FAM134B, SEC62, RTN3 and CCPG1) identified to be associated with the ER autophagy. Among these receptors, FAM134B, SEC62 and RTN3 have been reported to be closely related to the pathogenesis of HCC (Lin et al 2017;Du et al 2019;Zhang et al 2019). These lead us to investigate the possible clinicopathological and prognostic significance of CCPG1 in HCC.…”

Section: Introductionmentioning

confidence: 98%

Clinical and prognostic significance of CCPG1 in hepatocellular carcinoma

Wang,

Liu,

Wang

et al. 2023

gpb

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This study aimed to examine the clinical and prognostic significance of cell-cycle progression gene 1 (CCPG1) in hepatocellular carcinoma (HCC). We firstly analyzed CCPG1 expression in various cancers using The Cancer Genome Atlas and the Genotype-Tissue Expression project databases. The relative expression levels of CCPG1 were determined in 164 paired HCC and adjacent tissues using immunohistochemistry. The correlation between CCPG1 and clinicopathological characteristics of HCC was analyzed. Cox proportional models were used to identify the prognostic factors for overall survival (OS) and disease-free survival (DFS). The expression of CCPG1 was lower in HCC tissues than in adjacent non-tumor liver tissues. The expression of CCPG1 was significantly correlated with tumor number (p = 0.02) and tumor differentiation (p = 0.04) in HCC. Lower expression of CCPG1 in HCC patients was associated with poor OS and DFS (p < 0.01). Relative low expression of CCPG1 in HCC is significantly correlated with the poor prognosis of HCC patients after surgical resection, suggesting its possible role as a potential prognostic marker for HCC.

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Knockdown of Long Non-Coding RNA AFAP1-AS1 Promoted Viability and Suppressed Death of Cardiomyocytes in Response to I/R In Vitro and In Vivo

Chen

Wang

Hou

et al. 2020

J. of Cardiovasc. Trans. Res.

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Intrahepatic HCV RNA Level and Genotype 1 Independently Associate with Hepatic Reticulon 3 Expression

Abstract: Abstract. Background /Aim: Reticulon 3 (RTN3)

Cited by 3 publications

References 12 publications

Reticulon-3 modulates the incorporation of replication competent hepatitis C virus molecules for release inside infectious exosomes

Reticulon-3 modulates the incorporation of replication competent hepatitis C virus molecules for release inside infectious exosomes

Clinical and prognostic significance of CCPG1 in hepatocellular carcinoma

Knockdown of Long Non-Coding RNA AFAP1-AS1 Promoted Viability and Suppressed Death of Cardiomyocytes in Response to I/R In Vitro and In Vivo

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