An important mediator of gene expression that is increasingly understood is translational regulation. It gives cells the capacity to choose when to express a specific protein, ensuring appropriate and timely cellular responses to environmental signals. In complicated changing contexts, such as during embryonic development, wound healing, and environmental stress, this capacity to reprogram protein synthesis and to enable the translation of the relevant regulatory instructions is particularly crucial. It should come as no surprise that errors in this mechanism might cause cancer. This review will concentrate on the translational control mechanisms present in both healthy and malignant cells. We examine the idea that a change from capdependent to cap-independent signalling may contribute to the development of primary epithelial tumours into a motile mesenchymal-like phenotype during the invasive phase of metastasis. The mitochondria use phosphorylation to convert ADP to ATP to produce the vast majority of the energy required for cellular function. The formation of free radicals and apoptosis are two additional crucial mitochondrial processes. Numerous chemical substances, including those included in the current pharmacopoeia, have the potential to affect mitochondrial function. The inner mitochondrial membrane (IMM), which has electrochemical properties, the dual genetic control of mitochondrial DNA (mtDNA) and nuclear DNA (nDNA), as well as the inherent characteristics of the translational and transcriptional machinery, make the mitochondria vulnerable to environmental damage. Since mitochondria evolved from alpha-proteobacteria, the mtDNA genes are still structurally similar to the bacterial translational machinery, making them susceptible to inhibition by routinely used antibiotics that target translation. There are cases where certain gene mutations may lead to higher drug toxicity; however many of these drugs have side effects in otherwise healthy people. Personalized genomic medicine and preclinical pharmacogenetic and functional studies of mitochondrial toxicity are expected to advance our knowledge of the range of diseases induced by mitochondrial translation inhibition as well as the safe and efficient application of antibiotics that inhibit bacterial and human mitochondrial translation.