Abstract
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.
Highlights
Once thought to be transcriptional noise by virtue of their apparent inability to encode proteins, long non-coding RNAs have since emerged as vital regulators of gene expression
Over the past few years, there has been an unprecedented increase in the identification of dysregulated long non-coding RNAs (lncRNAs) in HBVrelated hepatocellular carcinoma (HCC)
Through an intricate network of interactions, involving epigenetic modifications to chromatin, modulation of transcription factors, sponging of miRNAs, protein interactions and miRNA production, these lncRNAs work in concert to promote tumorigenesis and cancer progression, while modulating hepatitis B virus (HBV) replication. Some of these lncRNAs are common to many other types of cancers, the manner in which an individual lncRNA functions sometimes varies across cancers
Summary
Once thought to be transcriptional noise by virtue of their apparent inability to encode proteins, long non-coding RNAs (lncRNAs) have since emerged as vital regulators of gene expression. LncRNAs are larger than 200 bases, a feature that distinguishes them from other non-coding RNAs, they may vary in size from a few hundred to a few thousand nucleotides These diverse molecules are encoded at various regions of the genome and can be classified according to their orientation in relation to the nearby protein coding genes [reviewed in [1]]. Certain lncRNAs, such as UCA1, DLEU2, HULC and DBHAS1, can be directly or indirectly upregulated by the HBV x (HBx) protein [8, 12, 18, 26] These lncRNAs may not necessarily be specific to HBV-related HCC as several, including those not induced by HBx, are commonly dysregulated in a variety of other cancers [5].
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