LncRNA MEG3 inhibits the growth, invasion and migration of Wilms' tumor via Wnt/β-catenin pathway.

Abstract

Long non-coding RNA (lncRNA) maternally expressed 3 (MEG3) has been identified to participate in the progression of malignant tumors. However, the role and function of MEG3 in Wilms' tumor (WT) remain unknown. Therefore, the aim of this study was to detect the role of MEG3 in the development of Wilms' tumor, and to explore the underlying mechanism. Expression of MEG3 in WT tissues and blood samples were detected using quantitative real-time polymerase chain reaction (qRT-PCR). The relationship between MEG3 level and clinicopathological character and histogenesis was analyzed. WT-CLS1 and WiT49 cells were cultured in vitro, and the influence of ectopic MEG3 expression was determined. Colony formation assay and Edu assay were employed to measure cell proliferation, while transwell assay and Matrigel assay were adopted to detect cell metastasis. Furthermore, Western blot was applied to explore the mechanism of MEG3 in WT. MEG3 was lowly expressed in WT tissues and blood samples (p<0.05). Over-expression of MEG3 significantly reduced the proliferation, invasion and migration of CLS1cells than control cells (p<0.05). However, inhibition of MEG3 in WiT49 cells significantly promoted cell growth and metastasis compared with cells in negative control group (p<0.05). In addition, MEG3 influenced the protein expression of β-catenin by regulating the Wnt/β-catenin pathway. MEG3 was low-expressed in WT tissues and blood samples. Meanwhile, it could inhibit the proliferation and metastasis of WT cells via wt/β-catenin pathways. All our findings indicated that MEG3 served as a potential target for the diagnosis, treatment and prognosis prediction of WT.