Reactive oxygen species: Friends or foes of lung cancer?

Abstract

Reactive oxygen species (ROS) are important biological radicals essential for determining different stages and phenotypes of cells from quiescence to proliferation, differentiation, self-renewal and even apoptosis. Low ROS favours quiescence and self-renewal in contrast to high ROS that dictates proliferation, differentiation or apoptosis. Such wide variety of cell fates depends upon specific signalling pathways that regulate the cellular ROS, thus contributing to tissue homeostasis. Imbalance of ROS causes several pathological conditions including cancer which is associated with higher level of ROS that supports tumour development and progression. However, to restrain from the excessive oxidative damage of ROS, cancer cells efficiently control the antioxidative pathways, thus favouring its own survival and maintenance at the same time. Furthermore, importance of ROS has been an active field of research in 'cancer stem cells' (CSCs), a subpopulation of cancer cells with stem cell-like properties and features. CSCs possess low ROS level that make them resistant to the existing chemotherapy or radiotherapy that ultimately leads to cancer recurrence. Though several evidences have proved the role of ROS in self-renewal and stemness of CSCs, there is a lot to explore about ROS-regulated signalling mechanisms in CSCs. An understanding of ROS regulation in CSCs can provide an idea about the application of oxidative stress as a therapeutic strategy in treatment of cancer. In this book chapter, we have raised the debate as to whether ROS acts as 'friend or foe' for cancer cells. Moreover, exploring the significance of ROS and redox regulation in lung cancer stem cells has been our major focus. Finally, it is suggested that in order to get an effective treatment and recurrence-free survival, sensitization of the cancer stem cells to high ROS environment is a must.