TRAIL gene therapy provides a promising therapy for the treatment of NSCLC.

MIH not only promotes the tumour-cell killing effect of radiotherapy through Bax-mediated cell death, but also improves cellular immunity in mice under radiotherapy and decreases the potential of radiotherapy to enhance MMP-9 expression, which leads to significant improvement in lung metastasis and overall survival of mice under combined treatment of MIH and R. This study is the first to have explored the effect of combined hyperthermia and radiotherapy on tumour metastasis and the underlying mechanisms. It provides insights into the application of MIH as an adjuvant to radiotherapy for metastatic breast cancer.

IntroductionReportedly, 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 methodsHuman 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.ResultsNF-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.ConclusionsThis study indicated that CBP-mediated NF-B p65 acetylation promotes the proliferation of NPC cells.