Dataset Information

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

ABSTRACT: 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.

SUBMITTER: Xing TR

PROVIDER: S-EPMC7074825 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

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

Xing Tian-Rong TR Chen Ping P Wu Jia-Mei JM Gao Li-Li LL Yang Wei W Cheng Yu Y Tong Li-Bo LB

OncoTargets and therapy 20200309

<h4>Background</h4>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 (<i>UPF1</i>) is an ATPase depending on RNA/DNA and RNA helicase depending on ATP. Long noncoding RNA (lncRNA) plasmacytoma variant translocation 1 (<i>PVT1</i>) was dysregulated in diverse diseases.<h4>Methods</h4>qRT-PCR and Western blot were applied to detect UPF1 and PVT1 in EC. CCK-8, colo ...[more]

PMID: 32210576

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Project description:Our previous study introduced the oncogenic role of the long non-coding RNA plasmacytoma variant translocation 1 (PVT1) in endometrial cancer (EC). In this study, we aimed to construct a PVT1-centered competing endogenous RNA (ceRNA) network to outline a regulatory axis that might promote the malignant progression of advanced EC. Raw Uterine Corpus Endometrial Carcinoma (UCEC) datasets were collected from The Cancer Genome Atlas (TCGA) database and used for construction of the PVT1-centered ceRNA network. The ceRNA binding sites were established using dual-luciferase assays. FISH assays displayed the co-location of PVT1 and miR-612 in EC cells. Immunohistochemistry, in situ hybridization, qRT-PCR, and western blots were used to assess the expression of miR-612 and CENP-H in EC tissues, and their functions on biological behaviours were examined by a series of in vitro and in vivo assays. Molecule interactions were illustrated by co-transfection assays. The bioinformatics analysis showed that PVT1/miR-612/CENP-H/CDK1 axis played a vital role in the malignant progression of advanced EC. MiR-612 was downregulated in EC tissues and acted as a tumour suppressor to inhibit cell proliferation, migration, invasion, and promote cell apoptosis. CENP-H was found overexpressed in EC tissues, and the expression level was correlated to diagnosis and prognosis of EC. Hyperactivated CENP-H promoted cell proliferation, migration, invasion, and inhibited cell apoptosis. Overexpressed CENP-H prevented the anti-tumour effects observed with upregulated miR-612; knockdown of miR-612 also suppressed the anti-tumour effects of downregulated PVT1. Knockdown of PVT1 together with upregulated miR-612 exerted the strongest anti-tumour effects in nude mice. These effects were mediated by CDK1 through modulation of the Akt/mTOR signaling pathway. In conclusion, the PVT1/miR-612/CENP-H/CDK1 axis promoted the malignant progression of advanced EC and could serve as a promising target for potential treatments.

Dataset Information

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

Publications

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

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