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. 2020 Jul 25;10(21):9443–9457. doi: 10.7150/thno.46078

Figure 1.

Figure 1

The implications of PARK2 in human ESCC samples and its effect on cancer-related phenotype in ESCC cell lines. A. PARK2 mRNA levels were significantly decreased in ESCC compared with matched adjacent non-tumor tissues. The data were obtained from TCGA database. B. PARK2 protein expression was significantly decreased in ESCC tissues compared with their adjacent non-tumor tissues as analyzed by IHC. C. Kaplan-Meier analysis revealed that low PARK2 expression was related with poorer overall survival of ESCC patients. P < 0.001, log-rank test. D. H & E staining was used to show different differentiation statuses of the ESCC (G1: high differentiation;G2: middle differentiation;G3:low differentiation). E. Immuno-blots showing CRISPR-mediated deletion of PARK2 in ESCC cell lines. F and G. PARK2 knockout promoted the migration and invasion in EC9706 cells (F) and KYSE150 cells (G) as determined by transwell assays. H and I. EC9706 cells (H) and KYSE150 cells (I) were labeled with EdU. EdU-positive cells, green; cell nuclei, blue; scale bar 100 µm. J. PARK2 knockout promoted the tumor growth of EC9706 cells in a xenograft model. The growth of xenografts was monitored over 5 weeks. Xenograft tumors were then dissected and their weights determined. K. Representatives and summary of migration and invasion assay showing that overexpression of PARK2 inhibited cell migration and invasion in EC9706 cells. L. PARK2 overexpression delayed the tumor growth of EC9706 cells in a xenograft model.