Although the major role of Nrf2 has long been established as a transcription factor for
providing cellular protection against oxidative stress, multiple pieces of research and reviews now
claim exactly the opposite. The dilemma - “to activate or inhibit” the protein requires an immediate
answer, which evidently links cellular metabolism to the causes and purpose of cancer. Profusely
growing cancerous cells have prolific energy requirements, which can only be fulfilled by modulating
cellular metabolism. This review highlights the cause and effect of Nrf2 modulation in cancer that in
turn channelize cellular metabolism, thereby fulfilling the energy requirements of cancer cells. The
present work also highlights the purpose of genetic mutations in Nrf2, in relation to cellular metabolism
in cancer cells, thus pointing out a newer approach where parallel mutations may be the key factor
to decide whether to activate or inhibit Nrf2.
Keywords: Nrf2, keap1, Reactive Oxygenation Species [ROS], cancer, oxidative stress, glycolysis, glutathione, Tricarboxylic
Acid Cycle [TCA], de novo lipogenesis.
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