Mechanism of LncRNA FTX regulates nephroblastoma progression through MiR-215-5p/PI3K/AKT axis

Abstract

Background: Nephroblastoma, also more commonly known as Wilms tumor (WT), is a common childhood malignancy that connects tumorigenesis and organ development in the kidney.

Objective: The current study focused on the effect of lncRNA FTX in nephroblastoma.

Study design: Expression of lncRNA FTX in nephroblastoma tissues and cells was determined. The expression location of lncRNA FTX was detected by FISH. The binding of lncRNA FTX and miR-215-5p with Ago2 was verified by RIP. Following gain- and loss-of-function approaches, the crucial role of lncRNA FTX and miR-215-5p in nephroblastoma cell functions was measured with the involvement of the PI3K/AKT pathway.

Results: LncRNA FTX was elevated and miR-215-5p was declined in nephroblastoma. Silencing of lncRNA FTX or mimic of miR-215-5p inhibited the malignant properties of nephroblastoma cells. LncRNA FTX was localized in the cytoplasm and might bind miR-215-5p. LncRNA FTX promoted the malignant features of nephroblastoma cells by inhibiting miR-215-5p through activating of the PI3K/AKT pathway.

Conclusions: LncRNA FTX is capable of accelerating nephroblastoma development in vitro by reducing miR-215-5p through activating of the PI3K/AKT pathway, indicating LncRNA FTX may possibly a future target for the diagnosis and treatment of nephroblastoma. SUMMARY FIGURE.

Keywords: LncRNA FTX; Nephroblastoma; PI3K/AKT; miR-215-5p.