上皮性卵巢癌中TFAP2A对hTERT表达的调节及其机制研究.

detected the expression level of TFAP2A and hTERT in normal ovarian epithelial tissues, borderline ovarian tumor tissues as well as epithelial ovarian cancer tissue by an IHC assay. The expression of TFAP2A gene in CAOV3 and SKOV3 cell lines were silenced by using small interfering RNA technique.The expression of TFAP2A in HO8910 cell line were overexpressed by overexpression plasmid. Western Blot and qRT-PCR were used to test the expression of hTERT in TFAP2A-silenced SKOV3 and CAOV3 cells or TFAP2A-overexpressed HO8910 cells. The relationship between TFAP2A, hTERT and PI3K/AKT signaling pathways was explored by using the agonist 740-YP and inhibitor LY294002 of the PI3K/AKT signalling pathway in TFAP2A-silenced CAOV3 cells or in TFAP2A-overexpressed HO8910 Result:. By immunohistochemistry assays, we found that TFAP2A was highly expressed in 71.88% epithelial ovarian cancer tissues, as well as hTERT was highly expressed in 78.12% of epithelial ovarian cancer tissues. By Pearson correlation analysis, We also found that the expression levels of hTERT were consistent with TFAP2A in different ovarian tissues, and the correlation coefficient was 0.78. Western Blot and qRT-PCR showed that the expression levels of hTERT was significantly decreased in TFAP2A-silenced CAOV3 and SKOV3 cells, while it was increased in TFAP2A-overexpressed HO8910. Western Blot showed that the hTERT would not significantly increased or decreased as the PI3K/AkT proteins after using PI3K/AkT signaling pathway agonist 740-YP or blocker LY294002. Conclusions: TFAP2A up-regulates hTERT expression in epithelial ovarian cancer cells do not by way of PI3K/AKT signaling. [ABSTRACT FROM AUTHOR]