Loss of vIRF1 reduces cell motility, invasion and proliferation induced by KSHV.

(A). Migration and invasion analyses of HUVECs treated with PBS (PBS) or infected with wild-type KSHV (KSHV_WT) or vIRF1 mutant virus (vIRF1_mut) followed by transduction with lentiviral vIRF1 at MOI 2 at 6 hpi. (B). Methylation-specific PCR showing DNA methylation of HUVECs treated as in (A). (C). Expression of lnc-OIP5-AS1, pre-miR-218-1 and miR-218-5p expression detected by qPCR in HUVECs treated as in (A). (D). Western-blotting of DNMT1, HMGB2 and CMPK1 expression in HUVECs treated as in (A). (E). Migration and invasion analyses of wild-type KSHV (KSHV_WT) cells, vIRF1 mutant cells (vIRF1_mut) or vIRF1-transduced mutant cells followed by transduction with a specific miR-218-5p inhibitor at 6 hpi. (F). Migration and invasion analyses of wild-type KSHV (KSHV_WT) cells, vIRF1 mutant cells (vIRF1_mut) or vIRF1-transduced mutant cells followed by transduction with lentiviral lnc-OIP5-AS1 (S3) construct and lentiviral lnc-OIP5-AS1 (S4) construct at 6 h. (G). A hypothetical model of the mechanism of how vIRF1 facilitates endothelial cell motility, invasion and proliferation. The quantified results represent mean ± SD. * P P P n.s, not significant.