Expression And Function Of Lrp16 In Ishikawa Human Endometrial Cancer Cells

Previous studies have demonstrated that LRP16 is an E2 responsive gene. Here, the regulation of LRP16 expression by E2 and the LRP16 function in Ishikawa cells were investigated. Northern blot and western blot were used to determine the gene expression levels. Cotransfection assays were used to determine the LRP16 promoter activity. The invasiveness of Ishikawa was evaluated by using the Matrigel-coated Transwell assay. E2 induced an increase in LRP16 mRNA levels in Ishikawa cells, whereas, its pure antagonist, ICI 182 780 reduced it. Ectopic ER transfection increased LRP16 expression. The significant increase of the LRP16 promoter-Luc activities in Ishikawa cells cotransfected with ER. Overexpression of LRP16 did not significantly affect growth rate of Ishikawa cells, but significantly increased the invasiveness. Ectopic LRP16 transfection markedly decreased the expression of E-cadherin. These studies demonstrated that estrogen up-regulated the LRP16 mRNA level by activation of ER. Up-regulation of LRP16 did not promote the proliferation of the endometrial cancer cells, but increased its invasive potential possibly by suppressing the E-cadherin expression level.