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. 2019 Apr 18;41(6):3292–3304. doi: 10.3892/or.2019.7131

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Copyright: © Zhang et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 4. — Silencing of USP9X in prostate cancer cell lines increases MMP9 protein level and mitochondrial fission. (A) A western blot analysis revealed that MMP9 and p-DRP1 protein levels were increased in USP9X-depleted LNCaP and PC-3 cells. No significant changes were observed in the levels of cyclin D1, E-cadherin and vimentin and total DRP1. (B) MitoTracker staining revealed that USP9X silencing induced mitochondrial fission in the prostate cancer cell lines. Relative mitochondrial length indicated the length of mitochondrial fragments in cells treated with siUSP9X relative to cells treated with siControl. The data are presented as the mean ± standard deviation (n=3). (C) JC-1 staining revealed no change in the mitochondrial membrane potential following USP9X silencing in prostate cancer cells. *P<0.05 vs. siControl, using Student's t-test. USP9X, ubiquitin-specific protease 9X; MMP9, matrix metalloproteinase 9; DRP1, dynamin-related protein 1; p-, phosphorylated; siUSP9X, siRNA targeting the USP9X gene; siControl, control siRNA.