Transcriptomic profiling of long non-coding RNAs in non-virus associated hepatocellular carcinoma

Liu, Lu; He, Chen; Liu, Haosheng; Wang, Ganlu; Lv, Zhiwu; Ni, Yicheng; Mou, Lisha; Yu, Zhan; Liu, Jintao

doi:10.1007/s12013-020-00915-4

Cited by 3 publications

(2 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The PacBio circular consensus sequencing reads analysed in this study have been previously published and can be found in the European Nucleotide Archive (PRJEB12450) [1]. The RNA-seq libraries of hepatitis B virus (HBV)-positive biopsy samples of human liver tumours and tissues, and portal vein tumour thrombosis (129, 182 and 92 libraries, respectively), and HBV-infected primary human hepatocytes (83 libraries) and human cultured cells HepaRG (4 libraries) and HepG2-NTCP (11 libraries) were downloaded from the Sequence Read Archive [2–18] (see the metadata in Table S1, available with the online version of this article).…”

Section: Data Summarymentioning

confidence: 99%

Quantitative analysis of the splice variants expressed by the major hepatitis B virus genotypes

et al. 2021

View full text Add to dashboard Cite

Hepatitis B virus (HBV) is a major human pathogen that causes liver diseases. The main HBV RNAs are unspliced transcripts that encode the key viral proteins. Recent studies have shown that some of the HBV spliced transcript isoforms are predictive of liver cancer, yet the roles of these spliced transcripts remain elusive. Furthermore, there are nine major HBV genotypes common in different regions of the world, these genotypes may express different spliced transcript isoforms. To systematically study the HBV splice variants, we transfected human hepatoma cells, Huh7, with four HBV genotypes (A2, B2, C2 and D3), followed by deep RNA-sequencing. We found that 13–28 % of HBV RNAs were splice variants, which were reproducibly detected across independent biological replicates. These comprised 6 novel and 10 previously identified splice variants. In particular, a novel, singly spliced transcript was detected in genotypes A2 and D3 at high levels. The biological relevance of these splice variants was supported by their identification in HBV-positive liver biopsy and serum samples, and in HBV-infected primary human hepatocytes. Interestingly the levels of HBV splice variants varied across the genotypes, but the spliced pregenomic RNA SP1 and SP9 were the two most abundant splice variants. Counterintuitively, these singly spliced SP1 and SP9 variants had a suboptimal 5′ splice site, supporting the idea that splicing of HBV RNAs is tightly controlled by the viral post-transcriptional regulatory RNA element.

show abstract

Section: Data Summarymentioning

confidence: 99%

Quantitative analysis of the splice variants expressed by the major hepatitis B virus genotypes

et al. 2021

View full text Add to dashboard Cite

show abstract

“…Since hepatitis virus-induced HCCs account for most cases, lncRNAs that are dysregulated in non-viral HCCs have not been fully investigated. A recent study shows that non-viral HCC also exhibits a differential expression profile when compared to hepatitis virus-induced HCC (48). However, lncRNAs such as HOTAIR and H19 have been found to be upregulated in obesity-induced HCC (49).…”

Section: Hepatitis B Virus (Hbv)-related Hepatocellular Carcinoma (Hcc) and Lncrna Dysregulationmentioning

confidence: 99%

Diversity of Dysregulated Long Non-Coding RNAs in HBV-Related Hepatocellular Carcinoma

et al. 2022

View full text Add to dashboard Cite

Infection with the hepatitis B virus (HBV) continues to pose a major threat to public health as approximately 292 million people worldwide are currently living with the chronic form of the disease, for which treatment is non-curative. Chronic HBV infections often progress to hepatocellular carcinoma (HCC) which is one of the world’s leading causes of cancer-related deaths. Although the process of hepatocarcinogenesis is multifaceted and has yet to be fully elucidated, several studies have implicated numerous long non-coding RNAs (lncRNAs) as contributors to the development of HCC. These host-derived lncRNAs, which are often dysregulated as a consequence of viral infection, have been shown to function as signals, decoys, guides, or scaffolds, to modulate gene expression at epigenetic, transcriptional, post-transcriptional and even post-translational levels. These lncRNAs mainly function to promote HBV replication and oncogene expression or downregulate tumor suppressors. Very few lncRNAs are known to suppress tumorigenesis and these are often downregulated in HCC. In this review, we describe the mechanisms by which lncRNA dysregulation in HBV-related HCC promotes tumorigenesis and cancer progression.

show abstract

Current mechanisms in obesity and tumor progression

Fosam

Perry

2020

Current Opinion in Clinical Nutrition &Amp; Metabolic Care

View full text Add to dashboard Cite

Purpose of review Hyperadiposity, as present in obesity, is a substantial threat to cancer risk and prognosis. Studies that have investigated the link between obesity and tumor progression have proposed several mechanistic frameworks, yet, these mechanisms are not fully defined. Further, a comprehensive understanding of how these various mechanisms may interact to create a dynamic disease state is lacking in the current literature. Recent findings Recent work has begun to explore not only discrete mechanisms by which obesity may promote tumor growth (for instance, metabolic and growth factor functions of insulin; inflammatory cytokines; adipokines; and others), but also how these putative tumor-promoting factors may interact. Summary This review will highlight the present understanding of obesity, as it relates to tumor development and progression. First, we will introduce the impact of obesity in cancer within the dynamic tumor microenvironment, which will serve as a theme to frame this review. The core of this review will discuss recently proposed mechanisms that implicate obesity in tumor progression, including chronic inflammation and the role of pro-inflammatory cytokines, adipokines, hormones, and genetic approaches. Furthermore, we intend to offer current insight in targeting adipose tissue during the development of cancer prevention and treatment strategies.

show abstract

Transcriptomic profiling of long non-coding RNAs in non-virus associated hepatocellular carcinoma

Cited by 3 publications

References 32 publications

Quantitative analysis of the splice variants expressed by the major hepatitis B virus genotypes

Quantitative analysis of the splice variants expressed by the major hepatitis B virus genotypes

Diversity of Dysregulated Long Non-Coding RNAs in HBV-Related Hepatocellular Carcinoma

Current mechanisms in obesity and tumor progression

Contact Info

Product

Resources

About