Skip to main content
. 2022 Mar 16;16(8):1694–1713. doi: 10.1002/1878-0261.13111

Fig. 7.

Fig. 7

MAPK/ERK signaling pathway plays a central role in UBE2T‐driven EMT. (A) Single CLSM sections after immunostaining of UBE2T overexpression clones (C1, C2) and controls (EV)‐embedded in Matrigel (3D) with SCH‐772984 inhibitor treatment. Scale bar: 10 μm. E‐cadherin: green, β‐catenin: red, DAPI: blue. (B) Scratch assay captured at 24 and 48 h of EV and UBE2T overexpression clones (C1, C2) with or without SCH‐772984 inhibitor treatment. Scale bar: 200 μm. (C) Quantification of gap closure at 24 and 48 h from (B). Data shown are representative from n = 5 independent experiments, two‐tailed Student's t‐test (*P ≤ 0.05, **P ≤ 0.01, ****P ≤ 0.0001). Empty vector (EV) stable cell lines were used as control for UBE2T overexpression stable cell lines (C1, C2).