Phosphatase of Regenerating Liver-3 Expression Correlates With PTENP1/miR-21 and miR-17/PTEN Dysregulation in Endometrial Adenocarcinoma Progression

Abstract

Background: Endometrial cancer is a prevalent gynecologic malignancy, which is predominantly of the histological type known as endometrial adenocarcinoma. Deletion of the tumor suppressor gene PTEN contributes significantly to the development of endometrial cancer. Phosphatase of regenerating liver-3 (PRL-3), as a common pro-oncogenic factor, has been shown to promote angiogenesis in endometrial cancer. However, the functional relationship between PRL-3 and phosphatase and tensin homolog deleted on chromosome 10 (PTEN) in endometrial cancer remains unclear.

Methods: Following the modulation of specific molecule expression, the levels of relevant molecules were assessed by quantitative real-time polymerase chain (qRT-PCR) and Western blot. Endometrial adenocarcinoma cell proliferation and migration were further determined by Cell Counting Kit-8 (CCK-8) assay and scratch assay.

Results: PTEN and phosphatase and tensin homolog pseudogene 1 (PTENP1) expression in endometrial adenocarcinoma samples and cell lines was analyzed and found to be closely associated with the malignant biological behavior of tumors. High expressions of PTENP1 and PTEN inhibited the proliferative and migratory capacities of endometrial adenocarcinoma cells, and high expressions of PRL-3, miR-21 and miR-17 enhanced their proliferative and migratory capacities. Bioinformatics analysis predicted that PTEN and PTENP1 were direct targets of miR-21 and miR-17. PRL-3 could downregulate PTENP1 and PTEN through upregulation of miR-21 and miR-17, which in turn could enhance the proliferative and migratory capacities of endometrial adenocarcinoma.

Conclusions: PRL-3 may play a pivotal role in promoting the proliferation and migration of endometrial adenocarcinoma by affecting the PTENP1/miR-21 or miR-17/PTEN.