KIAA0247 suppresses the proliferation, angiogenesis and promote apoptosis of human glioma through inactivation of the AKT and Stat3 signaling pathway
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Ying Tan1, Ning Huang1, Xiang Zhang1, Jiangang Hu1, Si Cheng2, Li Pi1, Yuan Cheng1
1Department of Neurosurgery, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China
2Department of Orthopaedics, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China
Yuan Cheng, email: [email protected]
Keywords: KIAA0247, glioma, cell proliferation, cell apoptosis, angiogenesis
Received: August 19, 2016 Accepted: November 02, 2016 Published: November 23, 2016
Gliomas are the most common and aggressive type of primary adult brain tumors. Although KIAA0247 previously is a speculated target of the tumor suppressor gene, little is known about the association between KIAA0247 and glioma. In this study, we clearly demonstrate that KIAA0247 expression is decreased in glioma and was negatively correlated with the histologic grade. Overexpression of KIAA0247 in glioma cells inhibits proliferation, angiogenesis and promoted apoptosis of human glioma cells in vitro. In contrast, knockdown of KIAA0247 increases the proliferation, angiogenesis and decreases apoptosis of these cells. In a tumor xenograft model, overexpression of KIAA0247 suppresses tumor growth of glioma cells in vivo, while KIAA0247 knockdown promotes the tumor growth. Mechanistically, overexpression of KIAA0247 is able to inhibit phosphorylation of AKT and Stat3 in glioma cells, resulting in inactivation of the AKT and Stat3 signaling pathways, this ultimately decreases the expression of PCNA, CyclinD1, Bcl2 and VEGF. Collectively, these data indicate that KIAA0247 may work as a tumor suppressor gene in glioma and a promising therapeutic target for gliomas.
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