LncRNA RNCR3 Promotes the Progression of HCC by Activating the Akt/GSK3β Signaling Pathway

• Published in: Evidence-based complementary and alternative medicine Vol. 2020; no. 2020; pp. 1 - 10
• Main Authors: Zhai, Lulu, Zhou, Chunhua, Ju, Tongfa, Xie, Qi
• Format: Journal Article
• Language: English
• Published: Cairo, Egypt Hindawi Publishing Corporation 2020; Hindawi; John Wiley & Sons, Inc; Hindawi Limited
• Subjects: AKT protein; Antisense RNA; Apoptosis; Axitinib; Cell adhesion & migration; Cell cycle; Cell growth; Cell migration; Cell proliferation; Development and progression; Ethics; Experiments; Hepatocellular carcinoma; Liver cancer; Medical prognosis; Metastases; Metastasis; NF-κB protein; Phosphorylation; Ribonucleic acid; RNA; Signal transduction; Survival analysis; Tumors; Japan; China; United States > US
• ISSN: 1741-427X; 1741-4288
• DOI: 10.1155/2020/8367454

Objective. To explore the potential biological roles of long noncoding RNA (lncRNA) RNCR3 in human hepatocellular carcinoma (HCC). Methods. First, the expression of RNCR3 was detected by qRT-PCR. Then, in vitro experiments were performed to investigate the effects of RNCR3 on the proliferation, cell cycle, migration, and invasion of HCC cells, while the effects of RNCR3 on HCC tumor growth and metastasis were investigated using in vivo experiments. Finally, western blot was used to study the activation of the Akt/GSK3β signaling pathway. Results. RNCR3 was highly expressed in both HCC tissues and cells, and the expression of RNCR3 was closely related to tumor size, tumor number, TNM stage, and overall survival time. In vitro, RNCR3 served as an oncogene to promote cell proliferation, migration, and invasion, and in vivo, RNCR3 promoted the growth and metastasis of HCC tumors. In terms of mechanism, RNCR3 induced the phosphorylation of Akt (thr308 and ser473) and GSK3β (ser9) but decreased the expression of GSK3β, which activated the Akt/GSK3β signaling pathway. Conclusion. The high expression of lncRNA RNCR3 in HCC can promote the proliferation, migration, invasion, growth, and metastasis of HCC by activating the NF-κB signaling pathway.