ArticleBioscience reports2016
Hepatitis C virus core protein impairs metabolic disorder of liver cell via HOTAIR-Sirt1 signalling.
Article in Bioscience reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
12 citing papers in PubMed, 24 citations in OpenAlex.
- Microscopic messengers: roles and prospects of extracellular vesicles in hepatitis B and C.Frontiers in immunology · 2026Review
- Dual roles and potential applications of exosomes in HCV infections.Frontiers in microbiology · 2022Review
- What role for cellular metabolism in the control of hepatitis viruses?Frontiers in immunology · 2022Review
- Article
- HOTAIR beyond repression: In protein degradation, inflammation, DNA damage response, and cell signaling.DNA repair · 2021Review
- LncRNAs in HCV Infection and HCV-Related Liver Disease.International journal of molecular sciences · 2020Review
- Long noncoding RNAs as regulators of cancer immunity.Molecular oncology · 2019Review
- Long noncoding RNAs in the metabolic control of inflammation and immune disorders.Cellular & molecular immunology · 2019Review
- Hepatitis C virus core impacts expression of miR122 and miR204 involved in carcinogenic progression via regulation of TGFBRAP1 and HOTTIP expression.OncoTargets and therapy · 2018Article
- Regulation of the Interferon Response by lncRNAs in HCV Infection.Frontiers in microbiology · 2018Review
- TAp73 is a marker of glutamine addiction in medulloblastoma.Genes & development · 2017Article
- Long Non-coding RNAs in Hepatitis C Virus-Infected Cells.Frontiers in microbiology · 2017Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It has been suggested that Hepatitis C virus (HCV) core protein is associated with metabolic disorders of liver cell. However, the precise mechanism is still unclear. The aim of the present study was to explore the impact of HCV core protein on hepatocyte metabolism by HepG2 and the possible involvement of long non-coding (lnc) RNAs in this process. The effect of HCV core protein on lncRNAs expression was examined with quantitative RT-PCR (qRT-PCR). Manipulation of HVC core protein and lncRNA HOTAIR was to evaluate the role of interaction between them on cell metabolism-related gene expression and cellular metabolism. The potential downstream Sirt1 signal was examined by western blotting and qRT-PCR. Our data suggested that suppression of HOTAIR abrogates HCV core protein-induced reduction in Sirt1 and differential expression of glucose- and lipid-metabolism-related genes. Also it benefits for metabolic homoeostasis of hepatocyte indicated by restoration of cellular reactive oxygen species (ROS) level and NAD/NADH ratio. By manipulation of HOTAIR, we concluded that HOTAIR negatively regulates Sirt1 expression through affecting its promotor methylation. Moreover, overexpression of Sirt1 reverses pcDNA-HOTAIR-induced glucose- and lipid-metabolism-related gene expression. Our study suggests that HCV core protein causes dysfunction of glucose and lipid metabolism in liver cells through HOTAIR-Sirt1 signalling pathway.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.