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. 2016 May 21;9:148–160. doi: 10.1016/j.ebiom.2016.05.025

Fig. 3.

Fig. 3

EBV infection leads to epithelial mesenchymal transition (EMT) and facilitates in vivo breast cancer formation. (A) Left: Two-dimensional morphology of EBV-infected (right in panel) versus GFP-control (left in panel). Right: Expression of Vimentin, E-cadherin, N-cadherin and Fibronectin as determined by quantitative RT-PCR of total RNA. Expression levels were normalized to GAPDH and displayed relative to the control cells. Bar graphs display results of experimental triplicates ± SD (B) Tumors generated from HMECs. Cells as indicated in the table were injected in the left (GFP-HMEC-R) or right (EBV-HMEC-R) flank of NOD/SCID mice. Tumors emerged only on the right (derived from EBV-HMEC-R) with a lag time of 12 weeks. (C) Growth curves of xenograft tumors generated from EBV-HMEC or GFP-HMEC. When injected at a dose of 2 × 107 in the left (GFP-HMEC-R) or right (EBV-HMEC-R) 4/5 injections resulted in tumors for each group. Displayed are the time of first palpation and the growth curves of the tumors. (D) Tumors were fixed, paraffin-embedded and stained with anti-Ki67 antibodies. The number of positive cells per high power field (HPF) was counted for each tumor in 3 different fields. * p ≤ 0.05 (two-sided T-test).