MIR562: Our studies have contributed to understanding the ANXA1-NF-κB signaling paradigm further, highlighted the regulation 2 miRNAs by ANXA1, namely miR26b* and MIR562 which directly targeted an NF-κB subunit REL-A (p65) and NF-κB1 (p105), respectively [PMC4275173]. With respect to MIR562, NF-κB1 and NF-κB activating protein were two NF-κB related genes predicted as targets [PMC4275173]. A decrease in fold-induction of NF-κB-promoter activity after PMA treatment was observed in cells over-expressing either miR26b* or MIR562, indicating that miR26b* and MIR562 was able to down-regulate NF-κB activity [PMC4275173]. Hence, the ANXA1-NF-κB signaling paradigm described previously by Bist et al has gained clarity with miR26b* and MIR562 being able to target p65 and p105 respectively [PMC4275173]. ANXA1 overexpression inhibits TNFα expression induced by MIR562, suggesting a role in regulating angiogenic activity [PMC4275173]. High levels of ANXA1 correlate with low levels of miR26b* and MIR562 [PMC4275173]. Transfection of MIR562 into ANXA1 overexpressing cells reverses the inhibition in migration observed with MIR562 alone [PMC4275173]. miR26b* and MIR562 have been shown to regulate endothelial cell tube formation in breast cancer cells [PMC4275173]. Both miR26b* and MIR562 inhibit NF-κB activity, leading to the down-regulation of NF-κB-dependent genes involved in wound healing/migration and angiogenesis [PMC4275173]. The expression levels of miR26b* and MIR562 are reduced when ANXA1 is high, suggesting a negative regulation by ANXA1 [PMC4275173]. The direct repression of NF-κB subunits RELA (p65) and NF-κB1 (p105) by miR26b* and MIR562 is associated with angiogenesis in breast cancer patients [PMC4275173].