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

被引：3

作者：

Ren W. ^{[1
]}

Ouyang L. ^{[2
]}

机构：

[1] Department of Gynecology and Obstetrics, General Hospital of Northern Theater Command, Shenyang

[2] Department of Gynecology and Obstetrics, Shengjing Hospital of China Medical University, Shenyang

来源：

Environmental Toxicology | 2024年 / 39卷 / 09期

关键词：

cancer progression; endometrial cancer; miR-187-3p; S100A4; VPS9D1-AS1;

D O I：

10.1002/tox.24351

中图分类号：

学科分类号：

摘要：

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. © 2024 Wiley Periodicals LLC.

引用

页码：4447 / 4458

页数：11

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