Downregulation of claudin-7 potentiates cellular proliferation and invasion in endometrial cancer

Claudin-7, a tight junction protein, has been demonstrated to be abnormally regulated in several types of human cancer. The present study aimed to investigate the expression and function of claudin-7 in endometrial cancer. In total, 31 pairs of endometrial cancer samples and their adjacent normal tissues were used to detect the expression of claudin-7 by immunohistochemical staining. Compared with the corresponding normal tissues, 45.2% of the endometrial cancer tissues exhibited weak or absent claudin-7 protein expression. Low levels of claudin-7 were correlated with a late tumor stage (P=0.023) and low histological grade (P=0.018). Claudin-7 was either overexpressed in AN3CA endometrial cancer cells, via plasmid cDNA transfection, or silenced by RNA interference in Ishikawa cells. Following either type of experimental manipulation, cellular proliferation and invasion were determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, wound healing and transwell assays, respectively. The silencing of claudin-7 significantly increased cellular proliferation (P=0.032) and invasion (P=0.020) rates. Consistent with these results, the increased expression of claudin-7 decreased the proliferation (P=0.021) and invasiveness (P=0.012) of the AN3CA cells. A low expression of claudin-7 in the endometrial cancer cells was indicative of a late tumor stage and low histological grade. Additionaly, restoration of claudin-7 inhibited the proliferation and invasion of endometrial cancer cells, thus providing a potential therapeutic strategy.