Objective      To investigate the role of human telomerase reverse transcriptase (hTERT) in intestinal metaplasia of gastric mucosa and the relevant molecular mechanism.       Methods      After the hTERT eukaryotic expression plasmids were successfully constructed

hTERT was transferred into human gastric cancer cell line MKN45 by lipofectamine 2000. Quantitative PCR and Western blotting were applied to examine the expression of the intestinal metaplasia genes

Cdx1

Cdx2 and Cdx4. Dual luciferase reporter assay was used to test the activity of the Cdx2 promoter. Furthermore

co-immunoprecipitation was employed to demonstrate the interaction between hTERT and p65. At last

NF-κB inhibitor was used to test the alleviation of the hTERT-induced Cdx2 promoter and protein expression.        Results      Quantitative PCR results showed that the expression of intestinal metaplasia genes Cdx1 and Cdx2 was up-regulated by hTERT

while Cdx4 gene had no obvious change. Western blot results verified that only Cdx2 protein level was increased. Dual luciferase reporter assay results demonstrated that hTERT promoted the activity of Cdx2 promoter. Moreover

co-immunoprecipitation results confirmed that hTERT protein could interact with p65 protein. Additionally

dual luciferase reporter assay and Western blot results revealed that NF-κB pathway inhibitor Bay78-1102 attenuated the activity of hTERT on Cdx2 promoter and down-regulated Cdx2 expression separately.       Conclusion      hTERT promotes the intestinal metaplasia of gastric mucosa via Cdx2 expression upregulation mediated by NF-κB pathway.