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Fig. 4 | Journal of Experimental & Clinical Cancer Research

Fig. 4

From: PRMT6-mediated transcriptional activation of ythdf2 promotes glioblastoma migration, invasion, and emt via the wnt–β-catenin pathway

Fig. 4

PRMT6 Interacts with CDK9 to Co-Regulate YTHDF2 Expression. A: Proteins specifically binding to PRMT6 in LN229 and U251 cell lines identified through mass spectrometry, intersected with transcription factors regulating YTHDF2 from the Cistrome database. B: Co-IP assay assessing the interaction between PRMT6 and CDK9 in LN229 and U251 cells. C-D: ChIP-PCR and ChIP-qPCR confirming the binding of PRMT6 and CDK9 to the YTHDF2 promoter region in LN229 cells. E: Dual-luciferase reporter assay in LN229 cells transfected with a YTHDF2 promoter-driven luciferase reporter plasmid, evaluating luciferase activity post overexpression or non-overexpression of PRMT6. F: Dual-luciferase reporter assay in HEK-293T cells, assessing luciferase activity after single or combined overexpression of PRMT6 and CDK9. G: Evaluation of CDK9 and YTHDF2 protein expression in LN229 and U251 cells with or without CDK9 knockdown. H: ChIP-qPCR analysis of CDK9 and PRMT6 binding to the YTHDF2 promoter region in LN229 cells with or without CDK9 knockdown. I: Dual-luciferase reporter assay in HEK-293T cells, measuring luciferase activity with PRMT6 knockdown, CDK9 overexpression, or CDK9 overexpression on a background of PRMT6 knockdown. J: Dual-luciferase reporter assay in HEK-293T cells, testing luciferase activity with CDK9 knockdown, PRMT6 overexpression, or PRMT6 overexpression on a background of CDK9 knockdown

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