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

Muhammad Javed Iqbal, Ayesha Kabeer, Zaighum Abbas, Hamid Anees Siddiqui, Daniela Calina, Javad Sharifi-Rad, William C Cho
Author Information
  1. Muhammad Javed Iqbal: Department of Biotechnology, University of Sialkot, Sialkot, Punjab, Pakistan.
  2. Ayesha Kabeer: Department of Biotechnology, University of Sialkot, Sialkot, Punjab, Pakistan.
  3. Zaighum Abbas: Department of Biotechnology, University of Sialkot, Sialkot, Punjab, Pakistan.
  4. Hamid Anees Siddiqui: Department of Biotechnology, University of Sialkot, Sialkot, Punjab, Pakistan.
  5. Daniela Calina: Department of Clinical Pharmacy, University of Medicine and Pharmacy of Craiova, 200349, Craiova, Romania. calinadaniela@gmail.com.
  6. Javad Sharifi-Rad: Facultad de Medicina, Universidad del Azuay, Cuenca, Ecuador. javad.sharifirad@gmail.com.
  7. William C Cho: Department of Clinical Oncology, Queen Elizabeth Hospital, Kowloon, Hong Kong. chocs@ha.org.hk.

Abstract

Cancer remains a significant global public health concern, with increasing incidence and mortality rates worldwide. Oxidative stress, characterized by the production of reactive oxygen species (ROS) within cells, plays a critical role in the development of cancer by affecting genomic stability and signaling pathways within the cellular microenvironment. Elevated levels of ROS disrupt cellular homeostasis and contribute to the loss of normal cellular functions, which are associated with the initiation and progression of various types of cancer. In this review, we have focused on elucidating the downstream signaling pathways that are influenced by oxidative stress and contribute to carcinogenesis. These pathways include p53, Keap1-NRF2, RB1, p21, APC, tumor suppressor genes, and cell type transitions. Dysregulation of these pathways can lead to uncontrolled cell growth, impaired DNA repair mechanisms, and evasion of cell death, all of which are hallmark features of cancer development. Therapeutic strategies aimed at targeting oxidative stress have emerged as a critical area of investigation for molecular biologists. The objective is to limit the response time of various types of cancer, including liver, breast, prostate, ovarian, and lung cancers. By modulating the redox balance and restoring cellular homeostasis, it may be possible to mitigate the damaging effects of oxidative stress and enhance the efficacy of cancer treatments. The development of targeted therapies and interventions that specifically address the impact of oxidative stress on cancer initiation and progression holds great promise in improving patient outcomes. These approaches may include antioxidant-based treatments, redox-modulating agents, and interventions that restore normal cellular function and signaling pathways affected by oxidative stress. In summary, understanding the role of oxidative stress in carcinogenesis and targeting this process through therapeutic interventions are of utmost importance in combating various types of cancer. Further research is needed to unravel the complex mechanisms underlying oxidative stress-related pathways and to develop effective strategies that can be translated into clinical applications for the management and treatment of cancer. Video Abstract.

Keywords

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MeSH Term

Humans
Reactive Oxygen Species
Kelch-Like ECH-Associated Protein 1
NF-E2-Related Factor 2
Oxidative Stress
Signal Transduction
Neoplasms
Oxidation-Reduction
Carcinogenesis
Tumor Microenvironment

Chemicals

Reactive Oxygen Species
Kelch-Like ECH-Associated Protein 1
NF-E2-Related Factor 2

Word Cloud

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