Insights into Metabolic Logic and Oxidative Stress in Cancer Using C. elegans

Main Article Content

Adina Fazyl

Center for Life Sciences, National Laboratory Astana, Nazarbayev University; Astana, 010000 Kazakhstan.

adina.fazyl@nu.edu.kz

Assiya Kukanova

Department of Biology, School of Sciences and Humanities, Nazarbayev University; Astana, 010000, Kazakhstan.

Department of Oncology, Astana Medical University, Astana 010000, Kazakhstan.

kukanova.a@amu.kz

Danysh Abetov

Center for Life Sciences, National Laboratory Astana, Nazarbayev University; Astana, 010000 Kazakhstan.

danysh.abetov@nu.edu.kz

Galiya Akylzhanova

Center for Life Sciences, National Laboratory Astana, Nazarbayev University; Astana, 010000 Kazakhstan.

galiya.akylzhanova@nu.edu.kz

Dos Sarbassov

Department of Biology, School of Sciences and Humanities, Nazarbayev University; Astana, 010000, Kazakhstan.

Center for Life Sciences, National Laboratory Astana, Nazarbayev University; Astana, 010000 Kazakhstan.

dos.sarbassov@nu.edu.kz

Dinara Begimbetova

Center for Life Sciences, National Laboratory Astana, Nazarbayev University; Astana, 010000 Kazakhstan.

dinara.begimbetova@nu.edu.kz

Abstract

This review examine the nematode Caenorhabditis elegans as a powerful model for cancer research, moving beyond its well-established utility in dissecting conserved genetic pathways. Its true strength may lie in modeling the intricate interplay between dysregulated metabolism and oxidative stress. This review first discusses how C. elegans  provides a whole-organism system to study the causal links between metabolic overload, the production of reactive oxygen species (ROS), and the activation of conserved detoxification pathways. The discussion then shifts to the Warburg effect, presenting the worm's unique rhodoquinone-dependent anaerobic metabolism as an evolutionary control experiment that offers a non-canonical framework for understanding the functional roles of lactate in the tumor microenvironment. Finally, this review examines the cell nucleus as an active sensor of stress, discussing how oxidative stress triggers the structural reorganization, from global chromatin remodeling to the formation of stress-induced biomolecular condensates. It is concluded that C. elegans  offers an excellent platform to progress from studying isolated cancer-related pathways toward an integrated understanding of the metabolic and environmental stress that drives tumorigenesis.

Keywords:
chromatin remodeling, oxidative stress, reactive oxygen species, Warburg effect, metabolic reprogramming, tumor model, Ras/MAPK signaling, apoptosis

Article Details

Received 2025-10-14
Accepted 2025-10-20
Published 2025-10-27

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