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UPF1 Participates in the Progression of Endometrial Cancer by Inhibiting the Expression of lncRNA PVT1

Authors Xing T, Chen P, Wu J, Gao L, Yang W, Cheng Y, Tong L

Received 1 October 2019

Accepted for publication 18 December 2019

Published 9 March 2020 Volume 2020:13 Pages 2103—2114

DOI https://doi.org/10.2147/OTT.S233149

Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 3

Editor who approved publication: Dr Leo Jen-Liang Su


Tian-rong Xing,1,* Ping Chen,1,* Jia-mei Wu,2 Li-li Gao,1 Wei Yang,1 Yu Cheng,1 Li-bo Tong1

1Department of Obstetrics and Gynecology, The First Affiliated Hospital of Jiamusi University, Jiamusi, Heilongjiang, People’s Republic of China; 2Department of Pathophysiology, School of Basic Medicine, Jiamusi University, Jiamusi, Heilongjiang, People’s Republic of China

*These authors contributed equally to this work

Correspondence: Li-bo Tong
Department of Obstetrics and Gynecology, The First Affiliated Hospital of Jiamusi University, 348 Dexiang Street, Jiamusi, Heilongjiang, People’s Republic of China
Email hljxingtianrong@sina.com

Background: Endometrial carcinoma (EC) is the primary cause of death associated with cancer globally. Thus, the possible molecular mechanism of EC needs further exploration. Up-frameshift protein 1 (UPF1) is an ATPase depending on RNA/DNA and RNA helicase depending on ATP. Long noncoding RNA (lncRNA) plasmacytoma variant translocation 1 (PVT1) was dysregulated in diverse diseases.
Methods: qRT-PCR and Western blot were applied to detect UPF1 and PVT1 in EC. CCK-8, colony formation, and Transwell assays were used to test the effects of UPF1/PVT1 on cell proliferation and migration. Cells were cultured with actinomycin D to observe mRNA stability, and RNA immunoprecipitation assay was applied to verified the relationship between UPF1 and PVT1. Glucose consumption and lactate generation were measured when cells were transfected with siRNA.
Results: Results demonstrated that the expression of UPF1 exhibited a remarkable decrement in EC tissues relative to that in non-tumor tissues. Subsequent functional experiments suggested that UPF1 decrement stimulated EC cells to grow and migrate. Moreover, UPF1 was discovered to be linked to PVT1 and had an inverse correlation with PVT1. Besides, PVT1 expression affected EC growth and migration, and PVT1 decrement alleviated the influence of UPF1 decrement on EC growth and migration and strengthened glycolysis in EC.
Conclusion: In this study, we found that UPF1 was down-regulated in EC tissues, and UPF1 might exert its role by regulating the expression of PVT1.

Keywords: endometrial carcinoma, UPF1, PVT1, cell growth, cell migration

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