Long non-coding RNAs in Epstein–Barr virus-related cancer

Abstract

Epstein Barr-virus (EBV) is related to several cancers. Long non-coding RNAs (lncRNAs) act by regulating target genes and are involved in tumourigenesis. However, the role of lncRNAs in EBV-associated cancers is rarely reported. Understanding the role and mechanism of lncRNAs in EBV-associated cancers may contribute to diagnosis, prognosis and clinical therapy in the future. EBV encodes not only miRNAs, but also BART lncRNAs during latency and the BHLF1 lncRNA during both the latent and lytic phases. These lncRNAs can be targeted regulate inflammation, invasion, and migration and thus tumourigenesis. The products of EBV also directly and indirectly regulate host lncRNAs, including LINC00312, NORAD CYTOR, SHNG8, SHNG5, MINCR, lncRNA-BC200, LINC00672, MALATI1, LINC00982, LINC02067, IGFBP7‐AS1, LOC100505716, LOC100128494, NAG7 and RP4-794H19.1, to facilitate tumourigenesis using different mechanisms. Additionally, lncRNAs have been previously validated to interact with microRNAs (miRNAs), and lncRNAs and miRNAs mutually suppress each other. The EBV-miR-BART6-3p/LOC553103/STMN1 axis inhibits EBV-associated tumour cell proliferation. Additionally, H. pylori–EBV co-infection promotes inflammatory lesions and results in EMT. HPV–EBV co-infection inhibits the transition from latency to lytic replication. KSHV–EBV co-infection aggravates tumourigenesis in huNSG mice. COVID-19–EBV co-infection may activate the immune system to destroy a tumour, although this situation is rare and the mechanism requires further confirmation. Hopefully, this information will shed some light on tumour therapy strategies tumourigenesis. Additionally, this strategy benefits for infected patients by preventing latency to lytic replication. Understanding the role and expression of lnRNAs in these two phases of EBV is critical to control the transition from latency to the lytic replication phase. This review presents differential expressed lncRNAs in EBV-associated cancers and provides resources to aid in developing superior strategies for clinical therapy.

SNHG8 Promotes the Progression of Epstein–Barr Virus-Associated Gastric Cancer via Sponging miR-512-5p and Targeting TRIM28

“…Cellular lncRNAs can be differentially induced by EBV infection. The dysregulated lncRNAs probably modulate tumorigenesis and other biological functions (28)(29)(30). Our result is consistent with others' reports that SNHG8 is associated with the progression in multiple types of cancer in the liver, colon, lung, ovary, prostate, esophagus, and so on (15,(31)(32)(33)(34)(35).…”

A comprehensive prognostic and immune analysis of enhancer RNA identifies IGFBP7-AS1 as a novel prognostic biomarker in Uterine Corpus Endometrial Carcinoma

“…In addition, further functional supported experiments demonstrated the knockdown of IGFBP7-AS1 inhibited the invasion and viability of U87 and U251 glioma cells (D. [24]. There were also results indicating that Epstein Barr-virus (EBV) may dysregulate host lncRNAs like IGFBP7-AS1 to regulate its own replication, thus facilitating tumorigenesis [27]. Although the IGFBP7-AS1's intervention in the progression of tumor proliferation and migration of few specific cancer types has been confirmed, we still lack of the mechanistic explanations for the prognostic ability of IGFBP7-AS1 in majority cancers, not to mention in UCEC.…”

Mono a Mano: ZBP1’s Love–Hate Relationship with the Kissing Virus

“…EBV has evolved other schemes to block cell death, including inhibition of apoptosis by latent membrane proteins (LMP), and small RNAs that target RIPK1/RIPK3 dependent pathways and not ZBP1 [ 62 , 63 ]. Additional EBV encoded genes suppress externally activated cell death pathways by blocking the expression of immunogenic viral genes on the PC surface [ 64 , 65 , 66 ]. While EBV has many ways to ensure the survival of infected PCs, blocking ZBP1 is not one of them.…”

“…In vitro assays confirm that EBV latency depends on the host encoded MYC and the FACT (Facilitates Chromatin Transcription) chromatin remodeler that is composed of SSRP1 (structure specific recognition protein 1) and SUPT16H (SPT16 homolog) subunits [ 66 , 72 , 91 , 92 , 93 ]. MYC works with FACT to suppress viral gene transcription.…”

“…Promoter usage can vary as well, leading to out-of-frame EBNA-LP RNAs that are non-protein coding. Potentially these transcripts could function as a ncRNA [ 120 ] that modulate both host and viral responses [ 66 ].…”