p16 and p21 act as tumor suppressors through induction of cellular senescence.  However, senescence-independent roles of these CDK inhibitors are not known.  To identify the mechanism responsible for the failure of Mo-MDSCs (monocytic myeloid-derived suppressor cells) infiltration into tumor allografts in p16/p21-double knockout (DKO) mice, we searched for chemokine receptors that were highly expressed in Mo- but not PMN-MDSCs (polymorphonuclear myeloid-derived suppressor cells) and were downregulated in p16/p21-DKO as compared to WT Mo-MDSCs. Ccr2, Ccr5, and Cx3cr1 were identified by RNA-seq analysis. SOURCE: Daisuke Okuzaki (dokuzaki@biken.osaka-u.ac.jp) -  RIMD, Osaka univ.

Pluto Bioinformatics

GSE93359: Transcriptome analysis of p16/p21-dependent monocytic myeloid-derived suppressor cells accumulation.