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. 2021 May 24;13(10):14015–14038. doi: 10.18632/aging.203012

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Copyright: © 2021 He et al.

This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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NUPR1 facilitated tumorigenesis of ccRCC in vitro. (A) Verification of NUPR1 mRNA and protein knockdown in ccRCC cell lines. (B) Cell growth curves of CCK-8 assay for ccRCC cell lines with NUPR1 silencing. (C) Colony formation assay for ccRCC cells with NUPR1 depletion. (D) The wound-healing assay of NUPR1 silencing on the migration of ccRCC cells. (E) Transwell experiment analysis of the effect of NUPR1 depletion on migratory and invasive abilities of ccRCC cells. (F) Effects of NUPR1 silencing on cell cycle regulation using flow cytometry. (G) Apoptosis assay of silencing NUPR1 in ccRCC by flow cytometry. (*p < 0.05, **p < 0.01, ***p < 0.001). CCK-8: cell counting kit-8; ccRCC: clear cell renal cell carcinoma.