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Fig. 3 | Molecular Cancer

Fig. 3

From: miR-508-3p concordantly silences NFKB1 and RELA to inactivate canonical NF-κB signaling in gastric carcinogenesis

Fig. 3

NFKB1 is a direct target of miR-508-3p in GC. a The binding site in the NFKB1 3'UTR for miR-508-3p as predicted by TargetScan (www.targetscan.org). b NFKB1 mRNA expression was down-regulated by ectopic miR-508-3p expression in MKN28, MGC-803 and SGC-7901 cells (**, P < 0.001). c Ectopic miR-508-3p expression decreased the RELA mRNA expression in GC cells (**, P < 0.001). d Both NFKB1 and RELA protein were down-regulated by miR-508-3p in three GC cell lines. e miR-508-3p overexpression inhibited the luciferase activity in the constructs containing wild type binding site, but the luciferase activity in the construct containing mutated binding site of NFKB1 3'UTR was not affected (Wild type, the construct containing the complementary sequence of seed region; Mutation, the binding site was deleted; **, P < 0.001). f ChIP-qPCR analysis on the promoter region of IL-1β and IL-6 after treating the cells with siNFKB1 or miR-508-3p. siNFKB1 or miR-508-3p decreased the binding affinity of NFKB1 on the promoter region of downstream targets IL-1β and IL-6 (**, P < 0.001). IP by IgG was as experimental negative control

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