Oncotarget

Research Papers:

HULC long noncoding RNA silencing suppresses angiogenesis by regulating ESM-1 via the PI3K/Akt/mTOR signaling pathway in human gliomas

Yu Zhu _, Xuebin Zhang, Lisha Qi, Ying Cai, Ping Yang, Geng Xuan and Yuan Jiang

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Oncotarget. 2016; 7:14429-14440. https://doi.org/10.18632/oncotarget.7418

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Abstract

Yu Zhu1,*, Xuebin Zhang2,*, Lisha Qi3,*, Ying Cai4, Ping Yang1, Geng Xuan5, Yuan Jiang6

1Department of Clinical Laboratory, Tianjin Huanhu Hospital, Tianjin Key Laboratory of Cerebral Vessels and Neural Degeneration, Tianjin, China

2Department of Pathology, Tianjin Huanhu Hospital, Tianjin Key Laboratory of Cerebral Vessels and Neural Degeneration, Tianjin, China

3Department of Pathology, Tianjin Medical University Cancer Institute and Hospital, The Key Laboratory of Tianjin Cancer Prevention and Treatment, Tianjin, China

4Tianjin Neurosurgery Institute, Tianjin Huanhu Hospital, Tianjin Key Laboratory of Cerebral Vessels and Neural Degeneration, Tianjin, China

5College of Clinical Laboratory, Tianjin Medical University, Tianjin, China

6Department of Immunology, Tianjin Key Laboratory of Cellular and Molecular Immunology, Key Laboratory of Educational Ministry of China, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China

*These authors contributed equally to this work

Correspondence to:

Yu Zhu, e-mail: [email protected]

Ping Yang, e-mail: [email protected]

Yuan Jiang, e-mail: [email protected]

Keywords: lncRNA, HULC, glioma, anoikis, proliferation

Received: October 06, 2015     Accepted: January 23, 2016     Published: February 15, 2016

ABSTRACT

Tumor angiogenesis plays a critical role in the tumor progression. Highly upregulated in liver cancer (HULC) is a long noncoding RNA (lncRNA) that acts as an oncogene in gliomas. We found that HULC, vascular endothelial growth factor (VEGF), and ESM-1 (endothelial cell specific molecule 1) expression and microvessel density were positively correlated with grade dependency in glioma patient tissues, and that HULC silencing suppressed angiogenesis by inhibiting glioma cells proliferation and invasion. This process induced anoikis and blocked the cell cycle at G1/S phase via the PI3K/Akt/mTOR signaling pathway, thus regulating the tumor-related genes involved in the above biological behavior in human glioma U87MG and U251 cells. However, these effects were reversed by ESM-1 overexpression, suggesting a mediating role of ESM-1 in the pro-angiogenesis effect of HULC. Our results define the mechanism of the pro-angiogenesis activity of HULC, which shows potential for application as a therapeutic target in glioma.


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