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Cancer Lett. 2016 May 28;375(1):100-107. doi: 10.1016/j.canlet.2016.02.044. Epub 2016 Mar 2.

SOX7 is associated with the suppression of human glioma by HMG-box dependent regulation of Wnt/β-catenin signaling.

Author information

1
Department of Neurosurgery, The Fourth Affiliated Hospital, Harbin Medical University, Harbin, China.
2
Department of Immunology, School of Basic Medical Sciences, Fudan University, Shanghai, China.
3
Department of Neurosurgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
4
Department of Clinical Laboratory, Beijing Shijiantan Hospital, Capital Medical University, Beijing, China.
5
Department of General Surgery, Shanghai Chang Zheng Hospital, Second Military Medical University, Shanghai, China.
6
Department of Neurosurgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, China. Electronic address: jiangchuanlusox@163.com.
7
Department of Neurosurgery, The Fourth Affiliated Hospital, Harbin Medical University, Harbin, China. Electronic address: liuxiaoqiansox@163.com.

Abstract

SOX7 has been recently recognized as a tumor suppressor belonging to the SOX (SRY-related HMG-box) family of a transcription factor. However, its role in human gliomas is unknown. Our study showed that SOX7 expression was significantly downregulated in human gliomas. Statistical analysis showed that SOX7 suppression was associated with higher histological grades of tumors in glioma tissues. SOX7 could suppress tumor properties both in vivo and in vitro, and depletion of the HMG domain abolishes its tumor suppressive roles. In vitro assays demonstrated that SOX7 could downregulate Wnt/β-catenin transcription and decrease the expression of Cyclin D1 and c-Myc, while the mutant SOX7 lost these functions. These results suggested that the HMG-box is a key domain of SOX7 for negatively regulating the Wnt/β-catenin signaling pathway when functioning as a tumor suppressor in a glioma.

KEYWORDS:

Glioma; SOX7; Tumor suppressor; Wnt/β-catenin

PMID:
26944317
DOI:
10.1016/j.canlet.2016.02.044
[Indexed for MEDLINE]

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