We aimed to measure ADAMTS18 expression in endometrial carcinoma (EC), atypical hyperplasia (AH), and normal endometrium, and determine its biological role in EC. Retrospectively, we analyzed clinicopathological data of the following groups: EC group (n = 64, endometrioid adenocarcinoma), AH group (n = 55), and control group (CON, n = 64, normal). ADAMTS18 expression was detected via immunohistochemical staining/immunofluorescence assay. Ishikawa EC cells were used in the following groups: ADAMTS18 group (overexpression plasmid), CON group (untreated), and NC group (null plasmid). The effects of ADAMTS18 on cell proliferation (CCK-8), migration/invasion (Transwell), and apoptosis (TUNEL) were assessed. ADAMTS18 expression was the lowest in the EC group and the highest in the CON group (P < 0.05). In Ishikawa cells, compared to the NC/CON groups, ADAMTS18 overexpression significantly decreased cell proliferation (after 72 h and 96 h), migration, and invasion, and enhanced cell apoptosis (all P < 0.05). Low ADAMTS18 expression was correlated with higher FIGO stage (≥ III) and larger tumor diameter (≥ 2 cm) in EC. ADAMTS18 downregulation was correlated with the poor prognosis of EC and suppressed tumor proliferation/invasion in vitro. ADAMTS18 overexpression modulated the behavior of EC cells by inhibiting their proliferation, invasion, and migration, and promoting their apoptosis. Functioning as a tumor suppressor, ADAMTS18 is a potential therapeutic target in EC.
Li et al. (Mon,) studied this question.