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HNRNPU Overexpression has Prognostic Value in Human Ovarian Cancer and Promotes Ovarian Cancer Cell Proliferation

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Abstract Background: Ovarian cancer (OC) is one of the most common gynecological malignancies and has the highest mortality rate worldwide. Therefore, the identification of novel targets and the development of more effective therapeutic treatments are essential.Methods: We identified genes with somatic copy number alterations (SCNAs) amplification (AMP) according to The Cancer Genome Atlas (TCGA) OC data. We performed a meta-analysis of five independent OC datasets from the Gene Expression Omnibus (GEO) database. We retrieved cell cycle-related genes from the online database GLAD4U. The associations of heterogeneous nuclear ribonucleoprotein U (HNRNPU) expression levels with clinicopathological factors and survival times were analyzed. In addition, we knocked down HNRNPU expression in two representative OC cell lines (OVCAR3 and ES2 cells) and then observed the proliferation capacity of OC cells.Results: Analysis of the SCNA AMP genes, the transcriptome data of the GEO database and cell cycle-related genes indicated that the HNRNPU gene was markedly upregulated in OC. High expression of HNRNPU in OC was related to SCNAs, poor survival and the OC proliferative molecular subtype. Based on the results in OVCAR3 and ES2 cells in vitro, we found that knocking down HNRNPU inhibited the proliferation of these two cell lines. Additionally, cell cycle arrest in the G1/S phase was found in the siHNRNPU cell group in vitro.Conclusions: These results suggest that HNRNPU may serve as a candidate prognostic marker and a potential therapeutic target for OC.
Title: HNRNPU Overexpression has Prognostic Value in Human Ovarian Cancer and Promotes Ovarian Cancer Cell Proliferation
Description:
Abstract Background: Ovarian cancer (OC) is one of the most common gynecological malignancies and has the highest mortality rate worldwide.
Therefore, the identification of novel targets and the development of more effective therapeutic treatments are essential.
Methods: We identified genes with somatic copy number alterations (SCNAs) amplification (AMP) according to The Cancer Genome Atlas (TCGA) OC data.
We performed a meta-analysis of five independent OC datasets from the Gene Expression Omnibus (GEO) database.
We retrieved cell cycle-related genes from the online database GLAD4U.
The associations of heterogeneous nuclear ribonucleoprotein U (HNRNPU) expression levels with clinicopathological factors and survival times were analyzed.
In addition, we knocked down HNRNPU expression in two representative OC cell lines (OVCAR3 and ES2 cells) and then observed the proliferation capacity of OC cells.
Results: Analysis of the SCNA AMP genes, the transcriptome data of the GEO database and cell cycle-related genes indicated that the HNRNPU gene was markedly upregulated in OC.
High expression of HNRNPU in OC was related to SCNAs, poor survival and the OC proliferative molecular subtype.
Based on the results in OVCAR3 and ES2 cells in vitro, we found that knocking down HNRNPU inhibited the proliferation of these two cell lines.
Additionally, cell cycle arrest in the G1/S phase was found in the siHNRNPU cell group in vitro.
Conclusions: These results suggest that HNRNPU may serve as a candidate prognostic marker and a potential therapeutic target for OC.

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