Aim
Glioma is the most common and malignant nervous system tumor and is associated with high-grade malignancy and high recurrence. The mammalian Dachshund1 (DACH1) is a recognized anti-tumor site and has low expression in several malignant tumors, including glioma. We designed and conducted this study to further determine the mechanism of DACH1 in glioma. Patients and
Conclusion
Downregulation of DACH1 was related to the malignancy and poor prognosis of patients with glioma, and DACH1 overexpression inhibited the tumor proliferation via the Wnt/β-catenin pathway. These findings might assist in the discovery of novel potential diagnostic and therapeutic targets for DACH1, thereby reducing the malignancy and recurrence of glioma.
Methods
The data collected from specimens of patients with glioma from GSE16011 and REMBRANDT databases were analyzed. The effect of DACH1 on proliferation, migration, and invasion of U87 and U251 cell lines was analyzed in vitro. The symbol targets of the Wnt/β-catenin pathway were also evaluated through Western blot.
Results
DACH1 deficiency was found in glioma tissues, and the DACH1 level was negatively correlated with the tumor malignancy. DACH1 overexpression inhibited the tumor proliferation, migration, and invasion. High expression of DACH1 also dampened the Wnt/β-catenin pathway, and the activation of the Wnt/β-catenin pathway partly led to the limited proliferation in glioma cells.