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Role of Stem Cells and Reactive Oxygen Species in Cancer

An Insight into Nrf2 Signaling

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Book cover Handbook of Oxidative Stress in Cancer: Therapeutic Aspects

Abstract

Cancer cells produce excessive reactive oxygen species (ROS) than normal cells because of their increased metabolism and mitochondrial dysfunction. Accumulation of intracellular ROS generation activates proto-oncogenes and inactivates the funtions of tumor suppressor gene. Intracellular ROS act as important signaling molecules to activate cancer cells proliferation and their metastasis. Nuclear factor erythroid 2-related factor 2 (Nrf-2) plays a crucial role by regulating the antioxidant genes expression. Nrf-2 activation intracellularly protects both normal and cancer cells from oxidative damage. Generally, intracellular ROS stimulate Nrf-2 signaling and increase the expression of cytoprotective antioxidant enzymes. In normal cells, enzymic antioxidants protect and nullify the intracellular oxidative imbalance. However, in tumor cells, oncogenic signaling activates Nrf-2 pathway, leading to tumor cells proliferation, drug resistance, stress adaptation, and activation of metabolic reprogramming. Nrf-2 activation has been reported in esophageal, liver, prostate, and breast cancer cells to defend the cancer cells against oxidant-induced cytotoxicity. Therefore, Nrf-2 inhibitors are used in anticancer agents. However, on the other hand, studies have shown that Nrf-2 transient expression is responsible to overcome chemical carcinogenesis. Nrf-2 signaling promotes proliferation, self-renewal, differentiation, and survival of cancer stem cells. On the other hand, stem cells transplantation has been tried for cancer therapy. Nrf-2 activation regulates self-renewal, quiescence, and regenerative potential of adult tissue stem cells and protects them from cellular stress and aging. Therefore, Nrf-2 activators are also reported to act as anticancer agents; however, Nrf2 activation is also a reason for cancer cells chemoresistance. Thus, the role of Nrf-2 signaling in cancer is remain inconclusive. 

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Authors and Affiliations

  1. Department of Pharmacology, The Blue Lab, Molecular Medicine and Toxicology Division, Saveetha Dental College, Saveetha Institute of Medical and Technical Sciences, Chennai, TN, India

    Devaraj Ezhilarasan & Perumal Elumalai

  2. Department of Genetics, Dr. ALM Post Graduate institute Basic Medical sciences, University of Madras, Chennai, TN, India

    Balakrishnan Anandan

  3. Department of Structural and Cellular Biology, Tulane University School of Medicine, New Orleans, LA, USA

    Anbalagan Muralidharan

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  1. Devaraj Ezhilarasan
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  2. Perumal Elumalai
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  3. Balakrishnan Anandan
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  4. Anbalagan Muralidharan
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Correspondence to Anbalagan Muralidharan .

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Editors and Affiliations

  1. Department of Biochemistry and Biophysics, University of Kalyani, Kalyani, West Bengal, India

    Sajal Chakraborti

Section Editor information

  1. Cellular Stress and Immune Response Laboratory, Centre for Cancer Biology, University of South Australia, Adelaide, South Australia, Australia

    Nirmal Robinson

  2. Department of Morphofunctional Sciences, "Grigore T. Popa" University of Medicine and Pharmacy, Iasi, Romania

    Cornelia Amalinei

  3. Department of Applied Biology, CSIR-Indian Institute of Chemical Technology, Hyderabad, Telangana State, India

    Amitava Das

  4. Biological Sciences, Academy of Scientific and Innovative Research, Ghaziabad,, UP, India

    Amitava Das

  5. Chettinad Hospital & Research Institute (CHRI), Chettinad Academy of Research and Education (CARE), Chennai, Tamil Nadu, India

    Surajit Pathak

  6. Stem Cell Facility, DBT-Centre of Excellence for Stem Cell Research, All India Institute of Medical Sciences, New Delhi, India

    Sujata Mohanty

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Ezhilarasan, D., Elumalai, P., Anandan, B., Muralidharan, A. (2022). Role of Stem Cells and Reactive Oxygen Species in Cancer. In: Chakraborti, S. (eds) Handbook of Oxidative Stress in Cancer: Therapeutic Aspects. Springer, Singapore. https://doi.org/10.1007/978-981-16-5422-0_103

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