CK2 Phosphorylates and Inhibits TAp73 Tumor Suppressor Function to Promote Expression of Cancer Stem Cell Genes and Phenotype in

Cancer stem cells (CSC) and genes have been linked to cancer development and therapeutic resistance, but the signaling mechanisms regulating CSC genes and phenotype are incompletely understood. CK2 has emerged as a key signal serine/ threonine kinase that modulates diverse signal cascades regulating cell fate and growth. We previously showed that CK2 is oftenaberrantly expressedand activated inheadandneck squamous cellcarcinomas (HNSCC), concomitantly with mutant (mt) tumorsuppressorTP53,andinactivation of its family member, TAp73. Unexpectedly, we observed that classical stem cell genes Nanog, Sox2 ,a ndOct4, are overexpressed in HNSCC with inactivate dT Ap73 and mtTP53. However, the potential relationship between CK2, TAp73 inactivation, and CSC phenotype is unknown. We reveal that inhibition of CK2 by pharmacologicinhibitorsorsiRNAinhibitstheexpressionofCSCgenesandsidepopulation(SP),whileenhancingTAp73mRNA