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Fig. 6 | Journal of Experimental & Clinical Cancer Research

Fig. 6

From: ARNTL hypermethylation promotes tumorigenesis and inhibits cisplatin sensitivity by activating CDK5 transcription in nasopharyngeal carcinoma

Fig. 6

CDK5 is a direct targeting gene of ARNTL. a ARNTL motif; b Putative ARNTL-binding sequence in promoter of CDK5 mRNA; c Spearman correlation analysis between ARNTL and CDK5 mRNA expression in GSE12452 nasopharyngeal carcinoma dataset; d Quantitative RT-PCR analysis of CDK5 mRNA expression in ARNTL-overexpression SUNE1 and HONE1 cells; e Quantitative RT-PCR analysis of CDK5 mRNA expression in ARNTL-silencing SUNE1 and HONE1 cells; f Western blotting analysis of CDK5 protein expression in ARNTL-overexpression or ARNTL-silencing SUNE1 and HONE1 cells;. g Relative luciferase activity of ARNTL-overexpression or Vector-expression SUNE1 and HONE1 cells after transfecting with wild type or mutant CDK5 3’UTR reporter genes. h ChIP real-time PCR assay for assessing the enrichment of ARNTL in the CDK5 promoter regimen in SUNE1-ARNTL and HONE1-ARNTL NPC cells (anti-RNA Pol II serves as positive control).; i Quantitative RT-PCR analysis of CDK5 mRNA expression in ARNTL-overexpression SUNE1 and HONE1 cells after transiently transfecting with CDK5-overexpression plasmid. j Western blotting analysis of CDK5 protein expression in ARNTL-overexpression SUNE1 and HONE1 cells after transiently transfecting with CDK5-overexpression plasmid. k The CCK-8 assay revealed overexpression of CDK5 could reverse ARNTL-mediated viability suppression in SUNE1 cells; l The CCK-8 assay revealed overexpression of CDK5 could reverse ARNTL-mediated viability suppression in HONE1 cells; (m-n) Colony formation assay revealed that CDK5 could reverse ARNTL-mediated colony-forming ability suppression in SUNE1 and HONE1 cells. * indicated P < 0.05; ** indicated P < 0.01

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