Fig. 4

Oncologic mutations or pathways revealed by ribosome profiling in malignancies. This figure summarizes some of the changes or mutations in oncologic pathways in cancer cells revealed by ribosome profiling. RPL22, a tumor suppressor maintaining the activity and stability of the p53 protein, is frequently mutated in cancers. YTHDF1, a m6A reader, boosts the translation of the p65 subunit of NF-κB to upregulate CXCL1 which supports MDSC migration via CXCL1-CXCR2 axis in CRCs, causing impaired antitumor immunity. A circRNA-encoded protein, C-HGF, induces the autophosphorylation and activation of c-MET, activating the downstream STAT3, AKT, and ERK signaling pathways, thus inducing the growth, migration and invasion of GBM. Another circRNA-encoded protein, circFGFR1p, antagonizes the pro-tumorigenic function of FGFR1. KRASIM and CIP2A-BP, encoded by lncRNAs, impair KRAS-induced ERK signaling activation and PI3K/AKT pathway, respectively. Similarly, METTL3 inactivates the PI3K/AKT signaling to inhibit differentiation but promote the proliferation of leukemia cells. Red arrows and blue “T” shapes stand for promotive and inhibitory effects respectively. Characters in blue or purple represent micropeptides/microproteins encoded by lncRNAs or circRNAs respectively