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Novel lncRNA SFTA1P Promotes Tumor Growth by Down-Regulating miR-4766-5p via PI3K/AKT/mTOR Signaling Pathway in Hepatocellular Carcinoma

Authors Huang G, Yang Y, Lv M, Huang T, Zhan X, Kang W, Hou J

Received 6 February 2020

Accepted for publication 22 July 2020

Published 30 September 2020 Volume 2020:13 Pages 9759—9770


Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 4

Editor who approved publication: Dr XuYu Yang

Guohong Huang,* Yimei Yang,* Mengxin Lv, Tian Huang, Xiaoyan Zhan, Wei Kang, Jianghou Hou

Clinical Research Center of Kunming Maternal and Child Health Hospital, Kunming 650031, People’s Republic of China

*These authors contributed equally to this work

Correspondence: Jianghou Hou
Clinical Research Center of Kunming Maternal and Child Health Hospital, Kunming 650031, People’s Republic of China
Email [email protected]

Background: Hepatocellular carcinoma (HCC) is a common malignancy worldwide with a high mortality rate. lncRNA SFTA1P is highly expressed in HCC. We aimed to study the role of SFTA1P in HCC and its relationship with miR-4766-5p.
Materials and Methods: The levels of SFTA1P in HCC tissues and cell lines were determined. Relationship between SFTA1P and clinical features and prognosis was studied. The influence of SFTA1P on HCC cell viability, migration, invasion and apoptosis was studied in vitro. Rescue experiments were conducted after the binding site between SFTA1P and miR-4766-5p confirmed by dual-luciferase assay. The protein expression of AKT, p-AKT, mTOR and p-mTOR in HCC cells with knockdown of SFTA1P was determined by Western blotting. A tumor study in nude mice was conducted in order to assess the effects of SFTA1P on tumor growth characteristics.
Results: SFTA1P was up-regulated in HCC tissues and cell lines. SFTA1P expression was closely related to tumor size, vascular invasion and TNM stage. Knockdown of SFTA1P inhibited HCC cell viability, migration and invasion and promoted cell apoptosis. MiR-4766-5p was a target of SFTA1P and knockdown of SFTA1P could decrease the protein expression of p-AKT and p-mTOR. Rescue experiments showed that miR-4766-5p mimics could attenuate the promoting role of SFTA1P on HCC cell viability, invasion and migration, and inhibiting role on cell apoptosis. Moreover, we used nude mice models and also found that the knockdown of SFTA1P reduced tumor volume and weight.
Conclusion: lncRNA SFTA1P could promote tumor development in HCC by down-regulating miR-4766-5p expression via PI3K/AKT/mTOR signaling pathway. It may be a potential therapeutic target for HCC.

Keywords: hepatocellular carcinoma, SFTA1P, miR-4766-5p, PI3K/AKT/mTOR signaling pathway, tumor growth

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