Knockdown of HDAC1 expression suppresses invasion and induces apoptosis in glioma cells
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Xiao-Qiang Wang1,*, Hong-Min Bai2,*, Shi-Ting Li1, Hui Sun1, Ling-Zhao Min1, Bang-Bao Tao1, Jun Zhong1 and Bin Li1
1Department of Neurosurgery, Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200092, China
2Department of Neurosurgery, Guangzhou General Hospital of Guangzhou Military Command, Guangzhou 510010, China
*These authors have contributed equally to this work
Shi-Ting Li, email: firstname.lastname@example.org
Bin Li, email: email@example.com
Keywords: glioma, HDAC1, proliferation, invasion, prognosis
Received: January 21, 2017 Accepted: April 29, 2017 Published: May 26, 2017
Glioma is the most common malignant tumor of the central nervous system, with a low survival rate of five years worldwide. Although high expression and prognostic value of histone deacetylase 1 (HDAC1) have been recently reported in various types of human tumors, the molecular mechanism underlying the biological function of HDAC1 in glioma is still unclear. We found that HDAC1 was elevated in glioma tissues and cell lines. HDAC1 expression was closely related with pathological grade and overall survival of patients with gliomas. Downregulation of HDAC1 inhibited cell proliferation, prevented invasion of glioma cell lines, and induced cell apoptosis. The expression of apoptosis and metastasis related molecules were detected by RT-PCR and Western blot, respectively, in U251 and T98G cells with HDAC1 knockdown. We found that HDAC1 knockdown upregulated expression of BIM, BAX, cleaved CASPASE3 and E-CADHERIN, and decreased expression of TWIST1, SNAIL and MMP9 in U251 and T98G cells with HDAC1 knockdown. In vivo data showed that knockdown of HDAC1 inhibited tumor growth in nude mice. In summary, HDAC1 may therefore be considered an unfavorable progression indicator for glioma patients, and may also serve as a potential therapeutic target.
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