Down-regulation of LncRNA NR027113 inhibits cell proliferation and metastasis via PTEN/PI3K/AKT signaling pathway in hepatocellular carcinoma

Z. Chen, Z.-Y. Zhou, C.-C. He, J.-L. Zhang, J. Wang, Z.-Y. Xiao

Guangdong Province Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Research Center of Medicine, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, China. jiewsysu@163.com

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• Oncology

OBJECTIVE: Hepatocellular Carcinoma (HCC) is a worldwide common and malignant tumor. It is discovered in recent years that long non-coding RNAs (lncRNAs) participate in many biological processes of HCC. However, their specific role in HCC has not been entirely clarified yet. In this research, we aimed to explore biological functions, clinical significance and the underlying molecular mechanisms of lncRNA NR027113 in HCC.

PATIENTS AND METHODS: qRT-PCR was performed to test the expression of NR027113 in HCC tissue samples and HCC cell lines. The association of NR027113 expression with overall survival, disease-free survival and clinicopathological factors was analyzed. MTT assays, Colony formation assay, flow cytometry and transwell invasion assays were performed to determine the effect of NR027113 in the regulation of biological behaviors of HCC cells. Western blot was performed to determine the activation of the PTEN/PI3K/AKT signaling pathway.

RESULTS: In the present study, we proved that is significantly up-regulated in HCC tissues and cell lines. HCC patients with higher NR027113 expression were associated with significantly shorter overall survival and disease-free survival. NR027113 knockdown inhibited the proliferation and metastasis of HCC cells in vitro. In addition, NR027113 knock-down was found to inhibit the activity of the PI3K/Akt signaling pathway and restrain the EMT process. Furthermore, we found that PTEN silencing could reverse the inhibitory effect of NR027113 knockdown on Akt phosphorylation and HCC cells function.

CONCLUSIONS: A brand new lncRNA NR027113 was found, which can promote the proliferation, invasion and metastasis of HCC via the PTEN/PI3K/AKT signaling pathway, and may be a potential therapeutic target in the future treatment of HCC.

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