Translation control of the immune checkpoint in cancer and its therapeutic targeting.

ABSTRACT: Cancer cells develop mechanisms to escape immunosurveillance, among which modulating the expression of immune suppressive messenger RNAs is most well-documented. However, how this is molecularly achieved remains largely unresolved. Here, we develop an in vivo mouse model of liver cancer to study oncogene cooperation in immunosurveillance. We show that MYC overexpression (MYC^Tg) synergizes with KRAS^G12D to induce an aggressive liver tumor leading to metastasis formation and reduced mouse survival compared with KRAS^G12D alone. Genome-wide ribosomal footprinting of MYC^Tg;KRAS^G12 tumors compared with KRAS^G12D revealed potential alterations in translation of mRNAs, including programmed-death-ligand 1 (PD-L1). Further analysis rev

SUBMITTER: Xu Y 

PROVIDER: S-EPMC6613562 | biostudies-literature | 2019 Feb

REPOSITORIES: biostudies-literature