J Cancer 2019; 10(13):2961-2968. doi:10.7150/jca.31004

Research Paper

Knockdown of linc01023 restrains glioma proliferation, migration and invasion by regulating IGF-1R/AKT pathway

Mingjun Yu1,2,3, Shijia Yu4, Wei Gong5, Duo Chen1,2, Junhong Guan1,2, Yunhui Liu1,2,3✉

1. Department of Neurosurgery, Shengjing Hospital of China Medical University, Shenyang 110004, People's Republic of China
2. Liaoning Clinical Medical Research Center in Nervous System Disease, Shenyang 110004, People's Republic of China
3. Key Laboratory of Neuro-oncology in Liaoning Province, Shenyang 110004, People's Republic of China
4. Department of Neurology, Shengjing Hospital of China Medical University, Shenyang 110004, People's Republic of China
5. Exprimental Research center, Shengjing Hospital of China Medical University, Shenyang 110004, People's Republic of China

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Citation:
Yu M, Yu S, Gong W, Chen D, Guan J, Liu Y. Knockdown of linc01023 restrains glioma proliferation, migration and invasion by regulating IGF-1R/AKT pathway. J Cancer 2019; 10(13):2961-2968. doi:10.7150/jca.31004. Available from http://www.jcancer.org/v10p2961.htm

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Abstract

LncRNAs have been proved to be involved in the promotion of glioma cell malignant development. However, the exact roles and molecular mechanisms of linc01023 in glioma remain blurred. In this study, we confirm linc01023 is up-regulated in glioma tissues and cell lines. In addition, elevated linc01023 expression indicates shorter survival times in patients with glioma. Moreover, loss-of-function studies reveal that restoration of linc01023 restrains glioma cell proliferation, migration and invasion by regulating IGF1R/AKT pathway in vitro and in vivo. Collectively, the study indicates that linc01023 plays an oncogenic role in glioma through activation of IGF1R/AKT signal pathway, and it could be a candidate therapeutic target.

Keywords: Glioma, Prognosis, Linc01023, IGF1R, AKT