Background: Esophageal cancer is one of the primary death causes leading by cancer in the world, which is high morbidity and mortality. Epigenetic acetylation modification participates in and regulates the proliferation, invasion, and metastasis of various tumor cells, and the acetylation modification of tumor proteins involved by acetyltransferases may be one of the important mechanisms of esophageal carcinogenesis. The aim of this study was to investigate the correlation of acetyltransferase P300 and Survivin acetylation in esophageal cancer pathogenesis and its molecular mechanism. Methods: Fifty-five cases of esophageal cancer tissues and adjacent cancer tissues were collected, Survivin and P300 protein expression was measured by immunohistochemistry (SP) and protein blotting (Western Blot); Survivin acetylated protein levels were measured by coimmunoprecipitation (Co-IP); bioinformatics predicted the relationship between P300 and Survivin as the substrate, and fluorescence immunohistochemistry (IF) to verify the localization and expression of Survivin and P300 in esophageal cancer tissues; the correlation of Survivin acetylation, P300 and clinical cases characteristics was analyzed by statistics. P300 siRNA sequences were structured and transfected into EC109 cells. P300 protein expression and Survivin acetylated protein levels were determined by Co-IP. Cell viability was determined by the MTT assay, Scratch healing and Transwell chamber assay examined cell migration and invasion ability. Results: Survivin and P300 protein expression was significantly increased in human esophageal cancer tissues and EC109 cells. The Survivin protein was acetylated in esophageal cancer tissues and EC109 cells, and its protein acetylation rate was significantly increased; bioinformatics predicted that the acetyltransferase P300 could catalyze the acetylation of Survivin as a substrate, and the fluorescence immunohistochemistry confirmed that both Survivin and P300 simultaneously showed a high expression state in cancer
Objective: To investigate the effect of Tip60 gene silencing on the ABCE1 acetylation level and cell proliferation, migration and invasion in TE-1 cells of oesophageal cancer. Methods: The siRNA sequence of Tip60 was transfected with esophageal cancer TE-1 cells. Transfected siRNA vector cells were used as experimental group (si-T), siRNA no-loaded somatic cells were transfected as control group (si-NC), and untransfected TE-1 cells were used as blank group (Group N). ABCE1 mRNA was detected by qRT-PCR, the expression of ABCE1 protein, proliferation-related protein β catenin (β-catenin), GSK3β, and c-myc by Western blot, the protein acetylation level by immunoprecipitation, MTT assay for cell viability, scratch healing and Transwell compartment assay for migration and invasion ability. Results: After 48 h downregulation of the Tip60 gene, TE-1 cells showed no significant changes in the ABCE1 mRNA and protein expression. The acetylation level of ABCE1 decreased significantly, compared with the control group and the blank group.After Tip60 gene silencing, the expression of β-catenin and c-myc protein decreased, while the expression of GSK-3β protein increased. Cytofunctology experiments showed that the proliferative activity, migration and invasion ability of TE-1 cells in the experimental group were significantly inhibited. Conclusion: Down regulation of Tip60 gene can deacetylate ABCE1 protein and inhibit the proliferation activity, migration and invasion ability of esophageal cancer by blocking the conduction of Wnt signaling pathway.
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