Overexpression of Nuclear Enriched Autosomal Transcript 1 Facilitates Cell Proliferation, Migration Invasion, and Suppresses Apoptosis in Endometrial Cancer by Targeting MicroRNA-202-3p/T Cell Immunoglobulin and Mucin Domain 4 Axis.

Abstract

Background: Endometrial cancer (EC) is an intractable gynecological cancer with increasing incidence and mortality worldwide. Accumulating studies indicated that long noncoding RNA nuclear enriched autosomal transcript 1 (NEAT1) was a novel oncogene implicated in a variety of cancers. However, whether NEAT1 could accelerate cell growth in EC is unclear. Materials and Methods: NEAT1, microRNA (miR)-202-3p, and T cell immunoglobulin and mucin domain 4 (TIMD4) levels were detected by quantitative real-time polymerase chain reaction. Cell proliferation and apoptosis were examined by cell counting kit-8 and flow cytometry. Transwell assay was employed for the evaluation of cell migration and invasion. The relationship between miR-202-3p and NEAT1 or TIMD4 was determined by luciferase reporter system. TIMD4 protein expression was assessed by Western blot assay. Results: NEAT1 was upregulated, whereas miR-202-3p was downregulated in EC tumors and cells. Depletion of NEAT1 restrained EC cell proliferation, migration, invasion, and improved apoptosis. MiR-202-3p was targeted by NEAT1 and could bind to TIMD4. Subsequently, it is observed that miR-202-3p inhibitor neutralized NEAT1 silencing mediated suppression on EC cell progression. Meanwhile, TIMD4 rescued miR-202-3p induced inhibition on cell progression in EC. Furthermore, it was obvious that NEAT1 facilitated TIMD4 expression by absorbing miR-202-3p in EC. Conclusions: Upregulation of NEAT1 accelerated EC cell progression through sponging miR-202-3p to facilitate TIMD4 expression, providing potential novel treatment method for EC.