This week Science published a short study examining the role of MYK in tumor immune evasion mechanisms [MYC is a transcription factor that regulates the expression of a multitude of gene products involved in cell proliferation, growth, differentiation, and apoptosis"].The authors found that MYK selectively directs expression of two immune-inhibitory molecules, CD47 and PD-L1, in several mouse and human tumor cells lines.
Using Tet-off transgenic mouse model to control MYK expression in T cell acute lymphoblastic leukemia (MYC T-ALL), the authors showed that both "in vitro or in vivo MYC inactivation resulted in a rapid downregulation of CD47 and PD-L1 [but not other surface markers], both at the mRNA level, as detected by quantitative real-time PCR (qPCR), and at the protein level, as detected by flow cytometry".
Since previous results demonstrated "complete tumor clearance following the inactivation of oncogenes, including MYC", the authors wanted to examine whether MYK effect on tumor regression involved CD47/PD-L1 tandem. Indeed, forced expression of either CD47 or PD-L1 in MYC T-ALL reduced anti-tumor effect of MYK inactivation.
In summary, this study suggests that MYK oncogene provides tumor cells with defenses to repel immune cells.