Long non‑coding RNAs in HBV‑related hepatocellular carcinoma (Review)

Zhang, Hao; Chen, Xuebing; Zhang, Jian; Wang, Xianwei; Chen, Huijuan; Liu, Lin; Liu, Shanling

doi:10.3892/ijo.2019.4909

Cited by 17 publications

(31 citation statements)

References 124 publications

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“…Some of these lncRNAs are discussed here. For a complete overview, the reader is referred to excellent recent reviews [ 291 , 305 , 318 , 319 , 321 , 322 , 326 ].…”

Section: Oncoviruses and Long Non-coding Rnasmentioning

confidence: 99%

“…HBx-LINE1 activated the Wnt signaling pathway by inducing nuclear localization of β-catenin, and stimulated cell proliferation and metastasis in vitro. An HBx-LINE1 transgenic mouse model revealed that the animals were more susceptible to diethylnitrosamine-induced tumor formation than wild-type mice and nuclear localization of β-catenin in hepatocytes of the transgenic animals was observed [ 305 , 319 , 321 , 322 , 323 , 326 ].…”

Section: Oncoviruses and Long Non-coding Rnasmentioning

confidence: 99%

“…Reduced expression of the lncRNAs n346077 and downregulated expression by HBx (DREH) was observed in HBV-positive HCC included. DREH inhibited proliferation and n346077 prevented migration and invasion in vitro [ 305 , 319 , 321 , 322 , 323 , 326 ].…”

Section: Oncoviruses and Long Non-coding Rnasmentioning

confidence: 99%

“…Studies with HBx expression in liver cell lines and with an HBx transgenic mouse model showed that HBx is directly involved in regulating lncRNA expression. HBx increased expression of HULC and HEIH [ 319 , 320 , 324 ]. HBx-induced upregulation of HULC is mediated by CREB, whereas HBx-induced expression of HEIH is mediated by transcription factor Sp1 [ 319 , 324 ].…”

Section: Oncoviruses and Long Non-coding Rnasmentioning

confidence: 99%

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Role of Virus-Induced Host Cell Epigenetic Changes in Cancer

Pietropaolo¹,

Prezioso

Moens

2021

IJMS

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The tumor viruses human T-lymphotropic virus 1 (HTLV-1), hepatitis C virus (HCV), Merkel cell polyomavirus (MCPyV), high-risk human papillomaviruses (HR-HPVs), Epstein-Barr virus (EBV), Kaposi’s sarcoma-associated herpes virus (KSHV) and hepatitis B virus (HBV) account for approximately 15% of all human cancers. Although the oncoproteins of these tumor viruses display no sequence similarity to one another, they use the same mechanisms to convey cancer hallmarks on the infected cell. Perturbed gene expression is one of the underlying mechanisms to induce cancer hallmarks. Epigenetic processes, including DNA methylation, histone modification and chromatin remodeling, microRNA, long noncoding RNA, and circular RNA affect gene expression without introducing changes in the DNA sequence. Increasing evidence demonstrates that oncoviruses cause epigenetic modifications, which play a pivotal role in carcinogenesis. In this review, recent advances in the role of host cell epigenetic changes in virus-induced cancers are summarized.

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“…Some of these lncRNAs are discussed here. For a complete overview, the reader is referred to excellent recent reviews [ 291 , 305 , 318 , 319 , 321 , 322 , 326 ].…”

Section: Oncoviruses and Long Non-coding Rnasmentioning

confidence: 99%

Section: Oncoviruses and Long Non-coding Rnasmentioning

confidence: 99%

Section: Oncoviruses and Long Non-coding Rnasmentioning

confidence: 99%

Section: Oncoviruses and Long Non-coding Rnasmentioning

confidence: 99%

See 2 more Smart Citations

Role of Virus-Induced Host Cell Epigenetic Changes in Cancer

Pietropaolo¹,

Prezioso

Moens

2021

IJMS

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“…More recently, HCC integrations have been found in TERT, MLL4, CCNE1, and CCNA2, etc. (e.g., [35,36]), mostly in promoter/intron regions, as well as in DNA sequences for non-coding RNAs [37]. However, unlike the situation in the woodchuck model, well-defined relationships between integration and tumorigenesis have been found in less than half of human HCCs analyzed so far.…”

Section: Hbv Dna Integration As a Risk Factor For Hccmentioning

confidence: 99%

Hepatitis B Virus DNA Integration and Clonal Expansion of Hepatocytes in the Chronically Infected Liver

Mason

Jilbert

Litwin

2021

Viruses

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Human hepatitis B virus (HBV) can cause chronic, lifelong infection of the liver that may lead to persistent or episodic immune-mediated inflammation against virus-infected hepatocytes. This immune response results in elevated rates of killing of virus-infected hepatocytes, which may extend over many years or decades, lead to fibrosis and cirrhosis, and play a role in the high incidence of hepatocellular carcinoma (HCC) in HBV carriers. Immune-mediated inflammation appears to cause oxidative DNA damage to hepatocytes, which may also play a major role in hepatocarcinogenesis. An additional DNA damaging feature of chronic infections is random integration of HBV DNA into the chromosomal DNA of hepatocytes. While HBV DNA integration does not have a role in virus replication it may alter gene expression of the host cell. Indeed, most HCCs that arise in HBV carriers contain integrated HBV DNA and, in many, the integrant appears to have played a role in hepatocarcinogenesis. Clonal expansion of hepatocytes, which is a natural feature of liver biology, occurs because the hepatocyte population is self-renewing and therefore loses complexity due to random hepatocyte death and replacement by proliferation of surviving hepatocytes. This process may also represent a risk factor for the development of HCC. Interestingly, during chronic HBV infection, hepatocyte clones detected using integrated HBV DNA as lineage-specific markers, emerge that are larger than those expected to occur by random death and proliferation of hepatocytes. The emergence of these larger hepatocyte clones may reflect a survival advantage that could be explained by an ability to avoid the host immune response. While most of these larger hepatocyte clones are probably not preneoplastic, some may have already acquired preneoplastic changes. Thus, chronic inflammation in the HBV-infected liver may be responsible, at least in part, for both initiation of HCC via oxidative DNA damage and promotion of HCC via stimulation of hepatocyte proliferation through immune-mediated killing and compensatory division.

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