DACH 1 inhibits glioma invasion and tumor growth via the Wnt/catenin pathway
Authors Wang J, Zou Y, Wu X, Chen M, Zhang S, Lu X, Wang Q
Received 18 April 2018
Accepted for publication 9 July 2018
Published 17 September 2018 Volume 2018:11 Pages 5853—5863
Checked for plagiarism Yes
Review by Single-blind
Peer reviewers approved by Dr Colin Mak
Peer reviewer comments 2
Editor who approved publication: Dr Federico Perche
Jing Wang,* Yan Zou,* Xuechao Wu, Mu Chen, Shuai Zhang, Xiaojie Lu, Qing Wang
Neurosurgery, The Affiliated Wuxi No 2 People’s Hospital, Nanjing Medical University, Wuxi, Jiangsu, People’s Republic of China
*These authors contributed equally to this work
Background/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 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.
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.
Keywords: DACH1, glioma, Wnt/catenin pathway, invasion, tumor growth
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