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Fig. 5 | Journal of Experimental & Clinical Cancer Research

Fig. 5

From: CircZNF215 promotes tumor growth and metastasis through inactivation of the PTEN/AKT pathway in intrahepatic cholangiocarcinoma

Fig. 5

PRDX1 is involved in cZNF215-mediated PTEN/AKT pathway inactivation by interacting with cZNF215. A RNA pull-down assays were performed using HuCCT1 cells lysates, following by mass spectrometry (MS) analysis. B MS analysis showing PRDX1 is likely to be a cZNF215-binding protein. C, D and E RNA pull-down and RNA immunoprecipitation assays analysis determined the interaction between cZNF215 and PRDX1 in indicated cells. F Immunoblot assays analysis revealing the expression of PRDX1, PTENred, PTENox, t-PTEN, p-AKTSer473/Thr308 and t-AKT in HuCCT1 cells transfected with vectors expressing PRDX1 or RBE cells transfected with PRDX1 siRNA. G and H Immunoblot assays analysis indicating the expression of PRDX1, PTENred, PTENox, t-PTEN, p-AKTSer473/Thr308 and t-AKT in HuCCT1 cells transfected with vectors expressing PRDX1 and treated with H2O2, or RBE cells transfected with PRDX1 siRNA and treated with NAC. I and J Western blot for the expression of PRDX1, p-AKTSer473/Thr308 and t-AKT in HuCCT1 cells cotransfected with indicated vectors or RBE cells cotransfected with indicated siRNAs. K and L Transwell assays analysis showing the migration and invasion capacity in iCCA cells. Scale bars, 200 μm. M CCK8 assays showing the proliferation ability of iCCA cells. Abbreviations: PTENred, reduced PTEN; PTENox, oxidized PTEN; t-PTEN, total PTEN; p-AKTSer473/Thr308, phosphorylation of AKT on Ser473 and Thr308; t-AKT, total AKT; NAC, N-acetylcysteine

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