Computational analysis of Epstein-Barr virus microRNA regulation on long non-coding RNAs in nasopharyngeal cancer

Abstract

Abstract To date, the regulatory framework mediated by Epstein-Barr virus (EBV) BART microRNAs (miRNAs) via their interaction with long non-coding RNAs (lncRNAs) in the context of nasopharyngeal cancer (NPC) pathogenesis remains partially understood. To derive a more complete insight into this phenomenon, we embarked on a computational study to identify BART miRNAs, lncRNAs, and all associate factors relevant to NPC tumourigenesis, and to characterise their interactions. In silico integration of multi-level RNA expression and construction of regulatory networks were performed. We found six EBV BART miRNAs (ebv- miR-BART21-3p, ebv-miR-BART19-3p, ebv-miR-BART15, ebv-miR-BART2-5p, ebv-miR-BART20-3p and ebv-miR-BART11-5p) that can interact with four messenger RNAs (mRNAs) (EYA4, EYA1, EBF1 and MACROD2) associated with NPC pathogenesis. These mRNAs can interact with six non-EBV miRNAs (hsa-miR-1246, hsa-miR-93-5p, hsa-miR-16-5p, hsa-miR-135b-5p, hsa-miR-211-5p and hsa-miR-1305), which in turn, could interact with three lncRNAs (CASC2, TPTE2P1 and ARHGEF26- AS1). These findings could shed light on the roles of dysregulated competing endogenous RNAs (ceRNA) network in NPC oncogenesis. In addition, we have also predicted the oncogenic and tumour suppressive functions of BART miRNAs and lncRNAs, and more precisely the involvement of BART miRNAs in DNA repair regulation and apoptosis.