HNRNPK and rhabdomyosarcoma: Gain- and loss-of-function experiments provided convincing evidence that pro-inflammatory lncRNA taurine upregulated 1 (TUG1) and rhabdomyosarcoma 2-associated transcript (RMST) trigger microglial polarization towards a pro-inflammatory (M1-like) phenotype by activation of the NF-κB pathway via competitive interaction with miR-145a-5p and heterogeneous nuclear ribonucleoprotein K (hnRNP K), respectively [357, 391].