LEF1 overexpression

We further showed that DDIAS downregulation inhibited cyclin A1, vimentin and the stemness-related factor CD133 and decreased the sphere formation capability, but these features were rescued by upregulation of LEF1. Taken together, these findings suggest that DDIAS promotes glioma progression and stemness by inducing LEF1 expression, proving that DDIAS may be a potential target for the treatment of glioma.

Down-regulation of Wnt antagonist secreted frizzled-related protein 4 (sFRP4) in GBM and GSCs, indicating activation of the Wnt/β-catenin pathway, which could be involved in the conversion of iPSCs to CSCs. From future perspectives, our study will help in the creation of a rapid cell-based platform for understanding the complexity of GBM.

In mice, NKTs expressing a GD2-specific chimeric-antigen receptor (CAR) with LEF1 demonstrated superior control of neuroblastoma xenograft tumors compared to control CAR-NKTs. These results identify LEF1 as a transcriptional activator of the NKT central memory program and advance development of NKT cell-based immunotherapy.

MiR-621 is a vital tumor suppressor in CRC and could be a promising anti-cancer therapeutic target.

LEF1 is a latent prognostic molecular biomarker of HCC. The cell cycle, and WNT and NOTCH signaling pathways are regulated by LEF1 in HCC. LEF1 could be a potential drug target for HCC.

This thesis concludes LEF1-AS1 may be an oncogenic lncRNA that regulates the target gene LEF1 by interacting with protein LEF1. However, the prognostic significance of lncRNA LEF1-AS1 in CLL patients is still unclear.

Eventually, LEF1 overexpression rescued cell progression impaired by MSC-AS1 knockdown. In summary, our research identified the MSC-AS1/miR-302a-3p/IGF2BP2/LEF1 axis in melanoma development, which indicated that MSC-AS1 is a potential biomarker in the treatment of melanoma.