Various research works have piled up conflicting evidence questioning the effect of oxidative stress in
cancer. Reactive
oxygen and
nitrogen species (RONS) are the reactive radicals and nonradical derivatives of
oxygen and
nitrogen. RONS can act as a double-edged weapon. On the one hand, RONS can promote
cancer initiation through activating certain signal transduction pathways that direct proliferation, survival, and stress resistance. On the other hand, they can mitigate
cancer progression via their resultant oxidative stress that causes many
cancer cells to die, as some recent studies have proposed that high RONS levels can limit the survival of
cancer cells during certain phases of
cancer development. Similarly, eukaryotic translation
initiation factors are key players in the process of cellular transformation and
tumorigenesis. Dysregulation of such translation
initiation factors in the form of overexpression, downregulation, or phosphorylation is associated with
cancer cell's altering capability of survival,
metastasis, and angiogenesis. Nonetheless, eIFs can affect
tumor age-related features. Data shows that alternating the eukaryotic translation initiation apparatus can impact many downstream cellular signaling pathways that directly affect
cancer development. Hence, researchers have been conducting various experiments towards a new trajectory to find novel therapeutic molecular targets to improve the efficacy of anticancer drugs as well as reduce their side effects, with a special focus on oxidative stress and initiation of translation to harness their effect in
cancer development. An increasing body of scientific evidence recently links oxidative stress and translation
initiation factors to
cancer-related signaling pathways. Therefore, in this review, we present and summarize the recent findings in this field linking certain signaling pathways related to
tumorigeneses such as MAPK and PI3K, with either RONS or eIFs.