Abstract

The purpose of this study was to illustrate the role of NAA10 in aggravating the malignant progression of renal cell carcinoma (RCC) by upregulating UPK1B. NAA10 levels in RCC tissues and paracancerous tissues were detected. Thereafter, the potential relationship between NAA10 level and clinical parameters of RCC patients was analyzed. After knockdown of NAA10, changes in proliferative potential of 786-O and Caki-1 cells were examined by cell counting kit-8 (CCK-8), colony formation and 5-Ethynyl-2'-deoxyuridine (EdU) assay. Finally, the regulatory role of NAA10 in the downstream gene UPK1B and the involvement of UPK1B in the development of RCC were determined via rescue experiments. NAA10 was upregulated in RCC tissues than paracancerous tissues. Tumor staging was much worse in RCC patients expressing a higher level of NAA10. Knockdown of NAA10 inhibited proliferative potential and downregulated UPK1B in RCC cells. Besides, NAA10 level was identified to be positively linked to UPK1B level in RCC tissues. At last, overexpression of UPK1B was able to abolish the inhibitory effect of silenced NAA10 on RCC proliferation. NAA10 level is closely linked to tumor staging and poor prognosis in RCC patients. NAA10 aggravates the malignant progression of RCC by upregulating UPK1B and may be a specific biomarker in RCC.

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