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. 2019 May 21;14(5):e0217037. doi: 10.1371/journal.pone.0217037

Fig 1. Suppressive effects of parkin KO on urethane-induced lung tumor development.

Fig 1

(A) Human normal lung or NSCLC tissue sections (Grade I–III) were processed and stained with H&E, and immunohistochemical analysis for the expression of parkin and p21 was performed. The figures represent 3 samples of each cancer stage. (B) Effect of IL-32γ on urethane-induced lung tumorigenesis in transgenic mice. The results are expressed as mean ± SD. * P < 0.05 compared with WT mice (n = 10). (C) Lung tumor tissue sections were analyzed by immunohistochemistry for the detection of parkin, PCNA, and p21 expression in the tumor tissues of parkin KO and WT mice. (D) The expression of parkin, p21, and PCNA was detected in the lung tumor tissues using specific antibodies. β-actin protein was used as an internal control. (E) Binding of parkin and p21 was detected using an immunoprecipitation assay (upper lane), while endogenous ubiquitination of p21 was detected through a ubiquitination assay (lower lane) in WT or parkin KO mice. Each band is representative of three independent experiments.