Expression of TCF3 in Wilms' tumor and its regulatory role inkidney tumor cell viability, migration and apoptosis invitro.

Abstract

Wilms' tumor (WT) is a major type of kidney cancer in children; however, the therapeutic measures for control of tumor metastasis, recurrence and death for this type of cancer remain unsatisfactory. The present study aimed to verify the expression of T-cell factor 3 (TCF3) in WT, and to explore its role in regulating the viability, migration and apoptosis of kidney tumor cells. Tumor tissues were collected from 10 patients with WT, and adjacent tissues were collected as normal controls. The expression levels of TCF3 were detected in WT tissues and adjacent tissues by reverse transcription-quantitative PCR (RT-qPCR), western blotting and immunohistochemistry. In addition, TCF3 expression was silenced in G401 kidney tumor cells via small interfering RNA transfection. Cell viability, cell cycle progression and cell apoptosis were assessed using the MTT assay and flow cytometry; the migration and invasion of kidney tumor cells were examined using Transwell and wound-healing assays; and the expression levels of Wnt signaling pathway-related genes (Wnt1, β-catenin and c-myc) were detected by RT-qPCR and western blotting. The results revealed that the expression levels of TCF3 were high in WT tissues from patients. Silencing TCF3 expression in G401 kidney tumor cells in vitro significantly inhibited cell viability and migration, and promoted cell apoptosis. Moreover, silencing TCF3 expression in G401 cells inhibited the expression levels of Wnt signaling pathway-related genes. Overall, these data indicated that TCF3 may be involved in WT development through regulation of Wnt signaling pathways. The findings of the present study provide a novel potential marker for the treatment and prognostic evaluation of WT.