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. 2013 Mar 1;14(3):262–270. doi: 10.4161/cbt.23299

graphic file with name cbt-14-262-g5.jpg

Figure 5. Schematic exhibition of the proposed signaling pathway modulated by CDH17 in gastric cancer cells. Coupling CDH17 activates the IKK complex, which subsequently phosphorylates the IκB-α. Then the phosphorylated IκB-α undergoes proteasome-dependent decomposition, which releases the heterodimers of p65/p50 into cytoplasm and transferred into the nucleus. Finally, the p65 binds to its responsive gene and promotes the transcription of downstream proteins including VEGF-C and MMP-9. On the other hand, RNAi mediated inhibition of CDH17 attenuates the activation of NFκB in gastric cancer cells, leading to a concomitant reduction in downstream proteins.