Long noncoding RNA VPS9D1‐AS1 promotes the progression of endometrial cancer via regulation of the miR‐187‐3p/S100A4 axis.

VPS9D1‐AS1 functions as an oncogene in many cancers. However, its role and potential mechanism in the progression of endometrial cancer (EC) are not fully understood. VPS9D1‐AS1 levels in EC and adjacent normal tissues were investigated using the TCGA‐UCEC cohort and 24 paired clinical samples. The roles of VPS9D1‐AS1 and miR‐187‐3p in cell cycle, proliferation, and apoptosis were evaluated by loss‐ and gain‐of‐function experiments. In addition, the effect of VPS9D1‐AS1 on tumor growth was further investigated in vivo. Rescue experiments were performed to investigate the involvement of the miR‐187‐3p/S100A4 axis in VPS9D1‐AS1 knockdown‐mediated antitumor effects. VPS9D1‐AS1 was highly expressed in EC tissues. VPS9D1‐AS1 knockdown, similar to miR‐187‐3p overexpression, significantly inhibited cell proliferation, inhibited colony formation, induced cell cycle arrest, and facilitated apoptosis of KLE cells. MiR‐187‐3p bound directly to VPS9D1‐AS1 and the 3′UTR of S100A4. Furthermore, VPS9D1‐AS1 negatively regulated miR‐187‐3p while positively regulating S100A4 expression in EC cells. MiR‐187‐3p knockdown or S100A4 overexpression partially reversed the tumor suppressive function of VPS9D1‐AS1 knockdown. The results suggest that VPS9D1‐AS1 affects EC progression by regulating the miR‐187‐3p/S100A4 axis. This may provide a promising therapeutic target to help treat EC. [ABSTRACT FROM AUTHOR]