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Background <p>Wilms tumor (WT) is a frequently diagnosed cancer in pediatric patients. DLX6-AS1 contributes to the emergence of several cancers. Nonetheless, the role of DLX6-AS1 in WT remains unclear. This study aimed to explore potential mechanisms by which DLX6-AS1 promotes the progression of WT.</p> Methods <p>DLX6-AS1, miR-195-5p, and kinesin family member 23 (KIF23) expression levels were measured by qRT-PCR in 22 pairs of tumor tissues and adjacent para-carcinoma tissues from WT patients, WT cell lines, and human renal tubular epithelial cell line (HK-2). The proliferation, migration and invasion, and epithelial-mesenchymal transition (EMT) like changes of WT cells were detected by CCK8, wound-healing, transwell assay and Western blotting.</p> Results <p>DLX6-AS1 was overexpressed 2–3 fold in WT tissues and cell lines compared to control tissues and cells. Silencing of DLX6-AS1 inhibited the proliferation of WT cells by 50%, and changed the expression of EMT related genes by 1.5 to 2 fold in WT cells. DLX6-AS1 acted as a sponge to upregulate the expression of KIF23 by recruiting miR-195-5p. The inhibition of miR-195-5p and overexpression of KIF23 partly reversed DLX6-AS1 silencing mediated suppression of migration, proliferation and EMT like changes of WT cells.</p> Conclusion <p>DLX6-AS1 could function as an oncogene to accelerate the development of WT by increasing the expression of oncogenic KIF23 by sponging miR-195-5p. DLX6-AS1/miR-195-5p/KIF23 axis is potential therapeutic target of WT.</p>

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DLX6-AS1 promotes the progression of Wilms tumor by sponging miR-195-5p to upregulate KIF23 in Wilms tumor cells

  • 期刊论文

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  • 发表日期：

    2026年5月19日

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  • Jiawei Chen,
  • Guowei Li,
  • Luqiu Chen,
  • Yunfeng Li,
  • Fengyin Sun

摘要

Background

Wilms tumor (WT) is a frequently diagnosed cancer in pediatric patients. DLX6-AS1 contributes to the emergence of several cancers. Nonetheless, the role of DLX6-AS1 in WT remains unclear. This study aimed to explore potential mechanisms by which DLX6-AS1 promotes the progression of WT.

Methods

DLX6-AS1, miR-195-5p, and kinesin family member 23 (KIF23) expression levels were measured by qRT-PCR in 22 pairs of tumor tissues and adjacent para-carcinoma tissues from WT patients, WT cell lines, and human renal tubular epithelial cell line (HK-2). The proliferation, migration and invasion, and epithelial-mesenchymal transition (EMT) like changes of WT cells were detected by CCK8, wound-healing, transwell assay and Western blotting.

Results

DLX6-AS1 was overexpressed 2–3 fold in WT tissues and cell lines compared to control tissues and cells. Silencing of DLX6-AS1 inhibited the proliferation of WT cells by 50%, and changed the expression of EMT related genes by 1.5 to 2 fold in WT cells. DLX6-AS1 acted as a sponge to upregulate the expression of KIF23 by recruiting miR-195-5p. The inhibition of miR-195-5p and overexpression of KIF23 partly reversed DLX6-AS1 silencing mediated suppression of migration, proliferation and EMT like changes of WT cells.

Conclusion

DLX6-AS1 could function as an oncogene to accelerate the development of WT by increasing the expression of oncogenic KIF23 by sponging miR-195-5p. DLX6-AS1/miR-195-5p/KIF23 axis is potential therapeutic target of WT.