Transcriptome profiling of PHGDH depleted mouse cancer cells under irradatioan treatment

irradiation (IR) triggers ZDHHC19-mediated palmitoylation of PHGDH (Phosphoglycerate dehydrogenase) at Cystine 396 and 225, resulting in YAP1 activation by PHGDH increased activity. Specifically, the PHGDH metabolite 3-phosphonooxypyruvate (3-PHP) allosterically blocks LATS1 kinase activity, thereby strongly preventing phosphorylation of YAP1 leading to fully activate YAP1. Dephosphorylated YAP1 in turn escorts PHGDH into the nucleus, where PHGDH undergoes K394 acetylation by P300 and converts alpha-ketoglutarate (alpha-KG) into D-2-hydroxyglutarate (D-2HG) which inhibits the activity of KDM2B leading to a global increase of H3K79me2 and an elevation of CCL20, CD24, and CXCL1 expression. Consequently, the abundant chemokines and surface molecules recruit neutrophils and macrophages into tumors, hindering cytotoxic T lymphocyte infiltration and promoting tumor evasion. The goal of the study is to profile the genes regulated by PHGDH in the mouse GC cells under irradiation treatment.