Research Papers:

The roles of ING5 in gliomas: a good marker for tumorigenesis and a potential target for gene therapy

Shuang Zhao, Zhi-Juan Zhao, Hao-Yu He, Ji-Cheng Wu, Xiao-Qing Ding, Lei Yang, Ning Jia, Zhi-Jie Li and Hua-Chuan Zheng _

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Oncotarget. 2017; 8:56558-56568. https://doi.org/10.18632/oncotarget.17802

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Shuang Zhao1, Zhi-Juan Zhao2, Hao-Yu He1, Ji-Cheng Wu1, Xiao-Qing Ding1, Lei Yang1, Ning Jia2, Zhi-Jie Li1 and Hua-Chuan Zheng1

1Department of Experimental Oncology and Animal Center, Shengjing Hospital of China Medical University, Shenyang 110004, China

2The First Affiliated Hospital of Jinzhou Medical University, Jinzhou 121001, China

Correspondence to:

Hua-Chuan Zheng, email: [email protected]

Keywords: glioma, ING5, tumorigenesis, chemotherapy, gene therapy

Received: December 16, 2016     Accepted: April 28, 2017     Published: May 11, 2017


To elucidate the anti-tumor effects and molecular mechanisms of ING5 on glioma cells, we overexpressed it in U87 cells, and examined the phenotypes and their relevant molecules. It was found that ING5 overexpression suppressed proliferation, energy metabolism, migration, invasion, and induced G2/M arrest, apoptosis, dedifferentiation, senescence, mesenchymal- epithelial transition and chemoresistance to cisplatin, MG132, paclitaxel and SAHA in U87 cells. There appeared a lower expression of N-cadherin, Twist, Slug, Zeb1, Zeb2, Snail, Ac-H3, Ac-H4, Cdc2, Cdk4 and XIAP, but a higher expression of Claudin 1, Histones 3 and 4, p21, p53, Bax, β-catenin, PI3K, Akt, and p-Akt in ING5 transfectants. ING5 overexpression suppressed tumor growth of U87 cells in nude mice by inhibiting proliferation and inducing apoptosis. Down-regulated ING5 expression was closely linked to the tumorigenesis and histogenesis of glioma. These data indicated that ING5 expression might be considered as a good marker for the tumorigenesis and histogenesis of gliomas. It might be employed as a potential target for gene therapy of glioma. PI3K/Akt or β-catenin/TCF-4 activation might be positively linked to chemotherapeutic resistance, mediated by ING5.

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