Oncogenic pathways and the electron transport chain: a dangeROS liaison

Vittoria Raimondi, Francesco Ciccarese, Vincenzo Ciminale

Research output: Contribution to journalReview articlepeer-review


Driver mutations in oncogenic pathways, rewiring of cellular metabolism and altered ROS homoeostasis are intimately connected hallmarks of cancer. Electrons derived from different metabolic processes are channelled into the mitochondrial electron transport chain (ETC) to fuel the oxidative phosphorylation process. Electrons leaking from the ETC can prematurely react with oxygen, resulting in the generation of reactive oxygen species (ROS). Several signalling pathways are affected by ROS, which act as second messengers controlling cell proliferation and survival. On the other hand, oncogenic pathways hijack the ETC, enhancing its ROS-producing capacity by increasing electron flow or by impinging on the structure and organisation of the ETC. In this review, we focus on the ETC as a source of ROS and its modulation by oncogenic pathways, which generates a vicious cycle that resets ROS levels to a higher homoeostatic set point, sustaining the cancer cell phenotype.

Original languageEnglish
Pages (from-to)168-181
Number of pages14
JournalBritish Journal of Cancer
Issue number2
Publication statusPublished - Dec 10 2019


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