Cancer Plasticity: The Role of mRNA Translation

Tumor progression is associated with dedifferentiated histopathologies concomitant with cancer cell survival within a changing, and often hostile, tumor microenvironment. These processes are enabled by cellular plasticity, whereby intracellular cues and extracellular signals are integrated to enable rapid shifts in cancer cell phenotypes. Cancer cell plasticity, at least in part, fuels tumor heterogeneity and facilitates metastasis and drug resistance. Protein synthesis is frequently dysregulated in cancer, and emerging data suggest that translational reprograming collaborates with epigenetic and metabolic programs to effectuate phenotypic plasticity of neoplasia. Herein, we discuss the potential role of mRNA translation in cancer cell plasticity, highlight emerging histopathological correlates, and deliberate on how this is related to efforts to improve understanding of the complex tumor ecology.

Automated summary

Tumor progression is associated with dedifferentiated histopathologies and cancer cell survival within a changing tumor microenvironment. Cellular plasticity enables rapid shifts in cancer cell phenotypes, fueling tumor heterogeneity, metastasis, and drug resistance. Dysregulated protein synthesis in cancer, along with translational reprogramming, epigenetic, and metabolic programs, contribute to the phenotypic plasticity of neoplasia.