EGF and gastric cancer: We found that mutation of the site A in the Wnt5a promoter significantly reduced the transcription activity by EGF stimulation and rescued by U0126 pretreatment (Figure 6E), indicating that binding of P-ERK to this site is critical for the transcriptional activation of Wnt5a. Specially, we noticed that an ERK mutant that is kinase-dead but retains the nuclear localization signal (NLS) (Figure 7A) could stay in the nucleus (Figure 7B) and still inhibit Wnt5a transcription (Figure 7C) as well as alter the expression of EMT markers (Figure 7D) in gastric cancer SGC-7901 cells.