Claudin-1 overexpression characterized type II (seropapillary) endometrial carcinoma, while claudin-2 was elevated in type I (endometrioid) carcinoma. Claudin-2 is a leaky type tight junction protein and overexpression of claudin-2 increases tumorgenesis of some type cancer cells. In the present study, we investigate the regulation and the role of claudin-2 in endometriosis and endometrioid carcinoma. In endometrioid carcinoma tissues, marked upregulation of claudin-2 was observed together with malignancy, while in endometriosis tissues, the changes in localization of claudin-2 was observed. The loss of claudin-2 by the siRNA upregulated the epithelial barrier and inhibited cell migartion in Sawano cells. Furthermore, the loss of claudin-2 affected cell cycle and inhibited cell proliferation. In Sawano cells cultured with high glucose medium, claudin-2 expression was downregulated at mRNA and protein levels. The high glucose medium upregulated the epithelial barrier and inhibited cell invasion. Histone deacetylase (HDAC) inhibitors tricostatin A and HDAC1 inhibitor which have antitumor effects, downregulated claudin-2 expression, cell proliferation, invasion and migration and upregulated the epithelial barrier. Taken together, overexpression of claudin-2 closely contributed to the malignancy of endometrioid carcinoma and downregulation of claudin-2 by the changes of glucose metabolism and HDAC might be important in therapy for cancer.
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