ESR2 and cancer: Besides being a target molecule for E2, via binding to ERb, which in turn regulates NDGR2 expression via transcriptional activation (53), it participates in other canonical and non-canonical pathways, such as CTNNB1 and NF-kb, respectively; both genes also present a TFBS for ESR2, which expression in this and other study (6) increases after day 40 p.o. In many malignant tumors, NGDR2 is able to suppress endothelial cell proliferation and enhance apoptosis by increasing p53 expression (54, 55).