HPV16 E6 increases cellular migration in EGF depleted cells.

<p>(<b>A</b>) Wound healing assays with primary HFKs stably expressing HPV16 E6 (E6) or infected with pLentiN6.3 control vector (C) following wounding of the cellular monolayer in the absence of EGF following RPTK and effector pathway inhibition. Cells were treated with DMSO or 100 nM Rapamycin, 1 µM Gefitinib, 150 nM OSI-906, or 10 µM U0126 and closure of the monolayer was measured over a 25 hour time course. Only images of the DMSO treated samples are shown (<b>B</b>). Quantification of wound closure as shown in (<b>A</b>). Surface areas of wounds were calculated relative to the surface area of the wounds at t = 0 hour. Bar represent averages and standard deviations of three experiments; asterisks indicate statistical significance (<i>P</i><0.0001). (<b>C</b>) Quantification of wound closure in the presence of 8 µg/ml Mitomycin C to inhibit cellular proliferation. (<b>D</b>) Quantification of wound closure in immortalized HFKs stably expressing HPV16 E6 (E6) or pLentiN6.3 control vector (C) (<b>E</b>). Transwell migration assay with HFKs stably expressing HPV16 E6 (E6) or pLentiN6.3 control vector (C). Cells were seeded in the absence of EGF on the top chamber of a transwell insert and migration to the bottom chamber in the absence of EGF was determined at 30 minutes and 60 minutes after seeding. The bars represent averages and standard deviations of three experiments; the asterisk indicates statistical significance (<i>P</i><0.05).