Mechanisms underlying the metastatic processes remain poorly understood. The epithelial-mesenchymal transition (EMT) programme is critically important in promoting pro-migratory and invasive properties that change the epithelial CD44-low cell state into a mesenchymal CD44-high state. EMT can be induced by a variety of physiological signals, causing pervasive reprogramming of both transcription and translation. Transcriptional changes are mediated, in part, by EMT-associated transcription factors, including ZEB1/2, Snail1/2, Smads and Twist1/2. The diverse repertoire of translated mRNAs in cancer cell plasticity and metastasis, however, remains unexplored. Towards unravelling this complex repertoire, we sought to examine dynamic changes in the translatome that occur as cancer cells change cell state during the EMT. We purified phenotypically distinct populations of HCC38 cells: poorly tumorigenic CD44-low (epithelial), intermediate CD44-low* (EMT programme initiated) and metastatic CD44-high (mesenchymal/stem-like cells). To detect and measure the transient translatome between cell populations, we will use RNA-Seq, Ribo-Seq and global proteome profiling. Preliminary RNA-Seq data has indicated preferential regulation of ribosome biogenesis across the different stages of EMT. Among the differentially expressed genes involved in transcription, maturation of ribosomal RNA (rRNA) and ribosome assembly are NOP10/56/58, BMS1, RRP1, RRBP1 and RRP36. High-throughput capture and analysis are underway to elucidate the mechanisms regulating the translatome that supports cancer cell plasticity and metastasis. Future work will focus on defining how the intertwined regulation of ZEB1 and ribosomal proteins promotes EMT and maintain the CD44-high cell state. Our study opens new avenues for exploiting therapeutic targets and developing future interventions to prevent metastatic spread and colonization in cancer patients.