Fig. 5: LINC00880 regulated PTEN-AKT pathway though forming a complex with CDK1 and PRDX1. | Cell Death & Disease

Fig. 5: LINC00880 regulated PTEN-AKT pathway though forming a complex with CDK1 and PRDX1.

From: The super-enhancer-driven lncRNA LINC00880 acts as a scaffold between CDK1 and PRDX1 to sustain the malignance of lung adenocarcinoma

Fig. 5

A Venn diagram showing the number of protein binding to CDK1 after LINC00880 overexpression (up panel). Changes of %Cov(95) (down panel). B Co-IP assays showed that endogenous CDK1 interacted with endogenous PRDX1, and LINC00880 enhanced the interaction between CDK1 and PRDX1. C PC9 cells were transfected with combinations of plasmids encoding Myc-PRDX1 and Flag-CDK1 followed by co-IP assays. D represent Immunofluorescence images showing the Co-localization of CDK1 and PRDX1 in LUAD tissues. E RNA pull-down and western blot assays were used to evaluate the interaction between LINC00880 and PRDX1. F RIP and qRT-PCR assays were used to measure the enrichment of LINC00880. G Immunoblot detection of the PRDX1 protein in PC9 cells as retrieved by in vitro transcribed biotinylated RNAs of different constructs of LINC00880 or its antisense sequence (as negative control). H RNA pull-down and western blot assays were used to evaluate the interaction between LINC00880 and flag-CDK1 and myc-PRDX1. I, J Western blotting detection of PRDX1, p-PRDX1, PTEN, AKT, p-AKT levels in PC9 cells transfected. The data are shown as the mean ± S.D. of at least three replicates (*P < 0.05, **P < 0.01, ***P < 0.001).

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