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Fig. 3 | Journal of Experimental & Clinical Cancer Research

Fig. 3

From: Current and future therapeutic strategies for high-grade gliomas leveraging the interplay between epigenetic regulators and kinase signaling networks

Fig. 3

Patterns of PRMT Methylation and Kinase Signaling Crosstalk. The PRMT family initiates distinct methylation patterns, including monomethylarginines, asymmetric dimethylarginines, and symmetric dimethylarginines, to epigenetically regulate cell processes. Highlighted are PRMT1, 2, 3, 5, and 6 which are associated with glioblastoma and medulloblastoma progression and/or tumorigenesis [30, 31, 51, 52, 118]. Functional genetic studies of PRMTs emphasize their modulation of kinase networks. For example, gene depletion of either PRMT2 or 5 is shown to decrease kinase signaling of both PI3K/AKT and MAPK pathways [31, 120]. Moreover, PRMT1 activates JAK/STAT3 pathway to promote cell differentiation, offering insights into potential PRMT-directed therapies [121]

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