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Reportedly, activation of the NF-B signaling pathway is related to the proliferation of nasopharyngeal carcinoma (NPC) cells; however, the underlying mechanism by which NF-B is activated in NPC cells is yet to be addressed. In our present studies, CREB-binding protein (CBP)-mediated acetylation of the NF-B p65 subunit and its effect on activation of NF-B p65 as well as its role in the proliferation of NPC cells were explored.    Material and methods  Human NPC cell lines CNE1 and C666-1 were cultured in vitro. The acetylation (Lys310) and phosphorylation (Ser536) levels of NF-B p65 in NPC cell lines were detected by Western blot. Then, the mRNA levels of CBP, p300, PCAF and GCN5 in NPC cell lines were determined by real-time PCR. Subsequently, the interaction of p65 with CBP in NPC cell lines was detected by a co-immunoprecipitation experiment. Furthermore, an NF-B p65 mutant (at Lys310), NF-B inhibitor and CBP shRNA were used to study the effect of CBP-mediated acetylation of NF-B p65 on the proliferation of NPC cell lines by CCK-8 assay.    Results  NF-B p65 was markedly acetylated at the site of Lys310 in NPC cells. Moreover, the mutation of NF-B p65 at the acetylation site markedly reduced proliferation of human NPC cells. Further investigation revealed that CBP was up-regulated and physically associated with NF-B p65 at the protein level in NPC cells. CBP-mediated NF-B p65 acetylation enhanced its phosphorylation and further contributed to the proliferation of NPC cells.    Conclusions  This study indicated that CBP-mediated NF-B p65 acetylation promotes the proliferation of NPC cells.

CBP-mediated acetylation of NF-κB p65 contributes to the proliferation of human nasopharyngeal carcinoma cells