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Erschienen in: Irish Journal of Medical Science (1971 -) 4/2022

31.08.2021 | Original Article

UBA2 promotes the progression of renal cell carcinoma by suppressing the p53 signaling

verfasst von: Xinbo Du, Jianguo Shi

Erschienen in: Irish Journal of Medical Science (1971 -) | Ausgabe 4/2022

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Abstract

Background

Renal cell carcinoma or RCC is a type of malignancy commonly occurred in the human kidney especially in the adults. The pathogenesis of RCC involves the complex networking of multiple signaling pathways, and the underlying molecular mechanisms remain largely unclear.

Objectives

This study aimed to elucidate the regulatory functions of UBA2 and explore its potential downstream molecules during the tumor progression in RCC.

Methods

In this paper, the expression of UBA2 and associated molecules was examined by RT-qPCR and western blotting. The proliferative activity of RCC cells was determined using CCK-8 assay and immunofluorescence staining of proliferation-related marker Ki-67. Moreover, the cell distribution and apoptosis were evaluated by flow cytometry.

Results

Our results revealed the upregulation of UBA2 in RCC tissues and cells, and the high-expression of UBA2 was also associated with bigger tumor size, more advanced stage, and poorer overall survival in RCC patients. In addition, UBA2 knockdown was able to suppress the growth of RCC cells and induced cell cycle arrest at G0/G1 phase. Furthermore, the p53 signaling could be the novel target of UBA2 in RCC, and UBA2 affected the biological behaviors of RCC cells in a p53-dependent manner.

Conclusion

In summary, UBA2 was able to enhance the proliferation, inhibit the apoptosis, and suppress cell cycle arrest in RCC cells by targeting the p53 pathway.
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Metadaten
Titel
UBA2 promotes the progression of renal cell carcinoma by suppressing the p53 signaling
verfasst von
Xinbo Du
Jianguo Shi
Publikationsdatum
31.08.2021
Verlag
Springer International Publishing
Erschienen in
Irish Journal of Medical Science (1971 -) / Ausgabe 4/2022
Print ISSN: 0021-1265
Elektronische ISSN: 1863-4362
DOI
https://doi.org/10.1007/s11845-021-02763-4

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