Suppressor of fused (Sufu) represses Gli1 transcription and nuclear accumulation, inhibits glioma cell proliferation, invasion and vasculogenic mimicry, improving glioma chemo-sensitivity and prognosis
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Xing Liu1,3,*, Xiaofeng Wang1,3,*, Wenzhong Du1,3,*, Lingchao Chen2, Guangzhi Wang1,3, Yuqiong Cui1,3, Yang Liu1,3, Zhijin Dou1,3, Hongjun Wang1,3, Ping Zhang1,3, Liang Chang1,3, Liye Yi1,3, Jinquan Cai1,3, Chuanlu Jiang1,3
1Department of Neurosurgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, China
2Department of Neurosurgery, Huashan Hospital, Fudan University, Shanghai, China
3Chinese Glioma Cooperation Group (CGCG)
*These authors contributed equally to this work
Chuanlu Jiang, e-mail: email@example.com
Lingchao Chen, e-mail: firstname.lastname@example.org
Keywords: glioma, Sufu, Gli1, temozolomide, hedgehog
Received: April 27, 2014 Accepted: October 10, 2014 Published: October 29, 2014
Glioblastoma are highly aggressive brain tumors with poor prognosis. While various dysregulation of signaling pathways in gliomas have been described, the identification of biomarkers and therapy targets remains an important task for novel diagnostic and therapeutic approaches. Here we described that the Suppressor of fused (also known as Sufu) is significantly down-regulated in high-grade gliomas, correlating with a poor prognosis. We demonstrated that ectopic expression of Sufu inhibited cell proliferation, invasion and vasculogenic mimicry. In addition, overexpression of Sufu reduced Gli reporter gene transcription activity and prevented Gli1 nuclear accumulation, whereas knockdown of Sufu reversed these effects. Furthermore, overexpressed Sufu sensitized glioblastoma to Temozolomide and Cyclopamine. Thus, Sufu is potential tumor suppressor and therapeutic target in glioblastoma.
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