Fig. 7: Model of the possible mechanism underlying G9A-induced metastasis in GC and the regulatory mechanism of G9A.
From: G9A promotes gastric cancer metastasis by upregulating ITGB3 in a SET domain-independent manner

Activation of p-ERK/p-SP1 by Reg IV in GC cells leads to the overexpression of G9A and the formation of a complex with P300 and GR in response to glucocorticoid stimulation, which results in increased ITGB3 expression and promotes the peritoneal metastasis of GC cells