Table 1 EBV genes, functional roles and their targets in gastric tumorigenesis.

EBER

Induces insulin growth factor 1 expression and promote cell proliferation

[115]

Induces chemoresistance and promotes cell migration

[116]

Downregulates mature miR-200 family thus to reduce E-cadherin expression

[117]

EBNA1

Causes the loss of PML NBs and impairs responses to DNA damage

[119]

Induces ROS accumulation to regulate cell viability

[120]

LMP2A

Activates NF-κB-survivin pathway to rescue EBV-infected epithelial cells from serum deprivation

[122]

Regulates cyclin E expression and S phase cell ratio

[123]

Elevates mitochondrial fission and promotes cellular migration through Notch pathway

[124]

Downregulates HLA to evade immune response

[125]

Activates phosphatidylinositol 3-kinase/Akt pathways to mediate transformation and inhibits transforming growth factor-beta 1-induced apoptosis

[126, 127]

Promotes cell malignant by inducing epigenetic changes of host genome

[129]

Upregulates miR-155–5p, and targets Smad2 and p-Smad2 to regulate TGF-β pathway

[128]

miR-BARTs

miR-BART9 decreases E-cadherin expression and upregulates proliferation

[133]

miR-BART3–3p inhibits the senescence of gastric cancer cells by targeting TP53

[134]

miR-BART5–3p targets the tumor-suppressor gene TP53, leading to acceleration of the cell cycle progress and inhibition of cell apoptosis

[135]

miR-BART5 targets PUMA, counteracts apoptosis and promotes cellular survival

[136]

miR-BART9, 11, and 12 downregulate Bim expression

[137]

miR-BART4–5p suppresses the proapoptotic protein Bid to regulate apoptosis

[138]

miR-BART20–5p interacts with 3’UTR of BAD to contribute to tumorigenesis

[139]

miR-BART16 suppresses type I IFN signaling

[140]