EBV epitranscriptome reprogramming by METTL14 is critical for viral-associated tumorigenesis

Lang, Fengchao; Singh, Rajnish Kumar; Pei, Yue‐Hu; Zhang, Shengwei; Sun, Kunfeng

doi:10.1371/journal.ppat.1007796

Cited by 97 publications

(120 citation statements)

References 42 publications

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“…Mechanistically, METTL14 contributes to oncogenesis through inducing m6A on the essential EBV latent antigen EBNA3C and thereby enhancing expression and stability of it. Interestingly, EBNA3C also increases expression and stability of METTL14 [54].…”

Section: Mettl14mentioning

confidence: 99%

Functions of N6-methyladenosine and its role in cancer

et al. 2019

Mol Cancer

916

816

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N6-methyladenosine (m6A) is methylation that occurs in the N6-position of adenosine, which is the most prevalent internal modification on eukaryotic mRNA. Accumulating evidence suggests that m6A modulates gene expression, thereby regulating cellular processes ranging from cell self-renewal, differentiation, invasion and apoptosis. M6A is installed by m6A methyltransferases, removed by m6A demethylases and recognized by reader proteins, which regulate of RNA metabolism including translation, splicing, export, degradation and microRNA processing. Alteration of m6A levels participates in cancer pathogenesis and development via regulating expression of tumor-related genes like BRD4, MYC, SOCS2 and EGFR. In this review, we elaborate on recent advances in research of m6A enzymes. We also highlight the underlying mechanism of m6A in cancer pathogenesis and progression. Finally, we review corresponding potential targets in cancer therapy.

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Section: Mettl14mentioning

confidence: 99%

Functions of N6-methyladenosine and its role in cancer

et al. 2019

Mol Cancer

916

816

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“…Dynamic and reversible m 6 A regulation was reported to be involved in various physiological and pathological processes including stem cell differentiation, cardiac homeostasis, adipogenesis, neuronal disorders, and spermatogenesis [15][16][17][18][19] . Recent years, compelling evidence has revealed that m 6 A modification plays an important role in the tumorigenesis of various cancers [20][21][22][23][24] . For example, METTL3 was reported to play key role in the progression of colorectal carcinoma 25 , bladder cancer 26,27 , gastric cancer 28 , and pancreatic cancer 29 .…”

Section: Introductionmentioning

confidence: 99%

WTAP promotes osteosarcoma tumorigenesis by repressing HMBOX1 expression in an m6A-dependent manner

Chen

Zhi³

et al. 2020

Cell Death Dis

100

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N 6-methyladenosine (m 6 A) regulators are involved in the progression of various cancers via regulating m 6 A modification. However, the potential role and mechanism of the m 6 A modification in osteosarcoma remains obscure. In this study, WTAP was found to be highly expressed in osteosarcoma tissue and it was an independent prognostic factor for overall survival in osteosarcoma. Functionally, WTAP, as an oncogene, was involved in the proliferation and metastasis of osteosarcoma in vitro and vivo. Mechanistically, M 6 A dot blot, RNA-seq and MeRIP-seq, MeRIP-qRT-PCR and luciferase reporter assays showed that HMBOX1 was identified as the target gene of WTAP, which regulated HMBOX1 stability depending on m 6 A modification at the 3′UTR of HMBOX1 mRNA. In addition, HMBOX1 expression was downregulated in osteosarcoma and was an independent prognostic factor for overall survival in osteosarcoma patients. Silenced HMBOX1 evidently attenuated shWTAP-mediated suppression on osteosarcoma growth and metastasis in vivo and vitro. Finally, WTAP/HMBOX1 regulated osteosarcoma growth and metastasis via PI3K/AKT pathway. In conclusion, this study demonstrated the critical role of the WTAP-mediated m 6 A modification in the progression of osteosarcoma, which could provide novel insights into osteosarcoma treatment.

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“…A research conducted by Zhang et al suggested that m6A modification was positively correlated with TMB/MSI status, and might be involved in immune responses of gastric cancer [ 61 ]. EBV-associated tumorigenesis has also been confirmed to require epitranscriptome reprogramming by METTL14 [ 82 ]. Thereby exploration of novel immunotherapy strategies targeting m6A is worth in-depth.…”

Section: Conclusion and Future Prospectusmentioning

confidence: 99%

Reshaping the role of m6A modification in cancer transcriptome: a review

2020

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N6-methyl-adenosine(m6A) modification emerges as an abundant and dynamic regulation throughout the Eukaryotic transcriptome. Dysregulation of the m6A regulators has increasingly been found in many neoplasms. It is reasonable to believe that m6A changes the fate of cancer cells and subsequently affected all aspects of cancer progression. In view of the context-dependent role of m6A modification, we emphasize a dual effect of m6A in a particular tumor model, that is, m6A plays a promoting role or a suppressing role in different stages of cancer. This novel sight is compared to the older view that a particular m6A regulator acts as a consistent role in cancer progression.

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EBV epitranscriptome reprogramming by METTL14 is critical for viral-associated tumorigenesis

Cited by 97 publications

References 42 publications

Functions of N6-methyladenosine and its role in cancer

Functions of N6-methyladenosine and its role in cancer

WTAP promotes osteosarcoma tumorigenesis by repressing HMBOX1 expression in an m6A-dependent manner

Reshaping the role of m6A modification in cancer transcriptome: a review

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