Effect of overexpressing HNRNPK in glioblastoma stem cell

The mechanisms underlys GBM cellular transitions remain unclear.In our study, we overexpressed HNRNPK in three different types of GSCs. HNRNPK (WT) leads to high expression of core markers in GSCs, and its characteristics are similar to those of the MES subtype, exhibiting stronger invasive abilities and tumorigenic potential. We mutated 422 site from lysine(K) to argnine(R) to study the function of SUMOylation in HNRNPK. Sequencing of GSCs with overexpression of HNRNPK (K422R) mutation confirmed the upregulation of infiltrating markers within the GSCs. The changes in GSC subtypes driven by overexpression of HNRNPK (WT or K422R) were not restricted by GSC mutation features. Overall design: To investigate the endogenous driving factors of GSC heterogeneity, we overexpressed wild-type HNRNPK or K422-mutated HNRNPK in three different types of GSCs.