AccScience Publishing / EJMO / Volume 8 / Issue 4 / DOI: 10.14744/ejmo.2024.20665
REVIEW

The FN3K-Nrf2 Axis: A Novel Therapeutic Target in Cancer  Metabolism

Erica Alves1 Gurupadayya Bannimath2* Prabitha Prabhakaran1 Narasimha Murthy Beeraka2,3,4
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1 Department of Pharmaceutical Chemistry, JSS College of Pharmacy, JSS Academy of Higher Education & Research, Mysore, India
2 Raghavendra Institute of Pharmaceutical Education and Research (RIPER), Anantapuramu, Chiyyedu, Andhra Pradesh, India
3 Department of Pediatrics, Herman B. Wells Center for Pediatric Research, Indiana University Faculty of Medicine, Indianapolis, USA
4 Department of Human Anatomy, I.M. Sechenov First Moscow State Medical University of the Ministry of Health of the Russian Federation (Sechenov University), Moscow, Russia
EJMO 2024, 8(4), 338–339; https://doi.org/10.14744/ejmo.2024.20665
Submitted: 5 July 2024 | Revised: 2 October 2024 | Accepted: 4 November 2024 | Published: 9 December 2024
© 2024 by the Author(s). This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution -Noncommercial 4.0 International License (CC-by the license) ( https://creativecommons.org/licenses/by-nc/4.0/ )
Abstract

Fructosamine-3-kinase (FN3K) is crucial for cellular metabolism, reversing early glycation products to maintain protein function and cellular homeostasis. Recent research highlights FN3K's role in cancer biology through its interaction with the Nrf2 transcription factor, which regulates cellular antioxidant responses and redox homeostasis. FN3K's deglycation activity can influence Nrf2 function, impacting cancer development and progression. Evidence suggests that FN3K stabilizes Nrf2, promoting the expression of genes involved in cell survival, proliferation, and chemotherapy resistance. Increased FN3K expression in cancers is linked to poor prognosis and treatment resistance, possibly by preventing Nrf2 ubiquitination and degradation. This sustained activation of Nrf2 target genes helps cancer cells bolster their antioxidant defenses and support tumor growth. Understanding the FN3K-Nrf2 interaction offers new therapeutic opportunities. Targeting FN3K-mediated deglycation could modulate Nrf2 activity in cancer, potentially enhancing treatment  efficacy and reducing resistance. Further research is needed to clarify the molecular mechanisms and develop specific 
inhibitors targeting FN3K in cancer cells. This review aims to provide an overview of FN3K, emphasize its importance in deglycation, and discuss pharmaceutical interventions targeting FN3K to combat cancer.

Keywords
Fructosamine-3-kinase (FN3K)
nuclear factor erythroid 2-related factor-2 (Nrf2)
deglycation
oncogenic
cancer
Conflict of interest
The authors declare they have no competing interests.
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