Interplay of oxidative stress, cellular communication and signaling pathways in cancer

Interplay of oxidative stress, cellular communication and signaling pathways in cancer

(2024) 22:7 | Muhammad Javed Iqbal1, Ayesha Kabeer1,2, Zaighum Abbas1, Hamid Anees Siddiqui1, Daniela Calina3*, Javad Sharifi-Rad4* and William C. Cho5*
Cancer remains a significant global health concern, with increasing incidence and mortality rates. Oxidative stress, characterized by the production of reactive oxygen species (ROS), plays a critical role in cancer development by disrupting genomic stability and cellular signaling pathways. Elevated ROS levels disrupt cellular homeostasis, leading to the loss of normal cellular functions and contributing to various types of cancer. This review focuses on the downstream signaling pathways influenced by oxidative stress, including p53, Keap1-NRF2, RB1, p21, APC, and tumor suppressor genes. Dysregulation of these pathways can lead to uncontrolled cell growth, impaired DNA repair, and evasion of cell death, all hallmarks of cancer development. Therapeutic strategies targeting oxidative stress have emerged as a critical area of investigation, aiming to limit cancer response times and enhance treatment efficacy. The review discusses the role of ROS in carcinogenesis and highlights the importance of understanding oxidative stress to develop effective therapeutic interventions. Various approaches, including antioxidant-based treatments, redox-modulating agents, and interventions to restore normal cellular function and signaling pathways, are explored. The interplay between oxidative stress and cellular pathways is crucial for advancing cancer management and treatment.Cancer remains a significant global health concern, with increasing incidence and mortality rates. Oxidative stress, characterized by the production of reactive oxygen species (ROS), plays a critical role in cancer development by disrupting genomic stability and cellular signaling pathways. Elevated ROS levels disrupt cellular homeostasis, leading to the loss of normal cellular functions and contributing to various types of cancer. This review focuses on the downstream signaling pathways influenced by oxidative stress, including p53, Keap1-NRF2, RB1, p21, APC, and tumor suppressor genes. Dysregulation of these pathways can lead to uncontrolled cell growth, impaired DNA repair, and evasion of cell death, all hallmarks of cancer development. Therapeutic strategies targeting oxidative stress have emerged as a critical area of investigation, aiming to limit cancer response times and enhance treatment efficacy. The review discusses the role of ROS in carcinogenesis and highlights the importance of understanding oxidative stress to develop effective therapeutic interventions. Various approaches, including antioxidant-based treatments, redox-modulating agents, and interventions to restore normal cellular function and signaling pathways, are explored. The interplay between oxidative stress and cellular pathways is crucial for advancing cancer management and treatment.
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