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Long noncoding RNA PVT1 promotes hepatoblastoma cell proliferation through activating STAT3

Authors Luo Z, Cao P

Received 27 April 2019

Accepted for publication 15 July 2019

Published 20 September 2019 Volume 2019:11 Pages 8517—8527

DOI https://doi.org/10.2147/CMAR.S213707

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Amy Norman

Peer reviewer comments 2

Editor who approved publication: Professor Nakshatri


Zhenqin Luo, Peiguo Cao

Oncology Department, The Third Xiangya Hospital of Central South University, Changsha, Hunan 410013, People’s Republic of China

Correspondence: Peiguo Cao
Oncology Department, The Third Xiangya Hospital of Central South University, 138 Tongzipo Road, Yuelu District, Changsha, Hunan 410013, People’s Republic of China
Email csucaopeiguo@126.com

Background: Hepatoblastoma is the most common liver malignancy in children. The long noncoding RNA (IncRNA) PVT1 plays oncogenic roles in human cancers; however, its regulation and function in hepatoblastoma remain poorly understood.
Purpose: This study was designed to investigate the regulation and function of PVT1 in hepatoblastoma.
Methods: PVT1 expression was compared between human hepatoblastoma tissues and adjacent non-tumor tissues, and then analyzed using Kaplan-Meier method. The proliferation of hepatoblastoma cells was determined by BrdU incorporation assay. The tumor xenograft model was used to assess tumor proliferation in vivo. The gene expression level was measured by qRT-pCR, Western blot and immunohistochemistry analyses.
Results: Compared with normal counterparts, PVT1 is upregulated in human hepatoblastoma tissues as well as in hepatoblastoma cell lines. Additionally, PVT1 promotes the proliferation of hepatoblastoma cells in vitro and accelerates tumor growth in xenograft model in vivo. Mechanistically, PVT1 promotes the activation of the signal transducer and activator of transcription 3 (STAT3), which leads to the transcriptional activation of downstream targets involved in cell cycle progression, and moreover,STAT3 inhibition with the selective inhibitor stattic abolishes PVT1 pro-proliferative role in hepatoblastoma cells.
Conclusion: PVT1 promotes hepatoblastoma cell proliferation through activating STAT3-induced cell cycle progression, which may implicate PVT1 as a potential therapeutic target for hepatoblastoma treatment.

Keywords: long noncoding RNA, PVT1, hepatoblastoma, proliferation, STAT3

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