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Telomere Maintenance and Metabolic Reprogramming in the Tumor Microenvironment
Special Issue Information
Dear Colleagues,
Telomere maintenance is increasingly recognized as a central hallmark of cancer, deeply intertwined with metabolic reprogramming in the tumor microenvironment (TME). While telomeres protect chromosomal ends and ensure genome stability, their dysfunction triggers DNA damage responses and senescence. Cancer cells bypass these barriers via telomerase reactivation or alternative lengthening of telomeres (ALT), supporting limitless replicative potential. Intriguingly, emerging evidence suggests that telomere maintenance mechanisms (TMMs) do not act in isolation but dynamically interact with metabolic circuits and inflammatory responses that shape the TME—such as glycolysis, oxidative phosphorylation, lipid biosynthesis, redox balance, and senescence-associated secretory phenotypes (SASPs).
Oncogenic metabolism supports telomere homeostasis by modulating nucleotide pools, reactive oxygen species (ROS), and epigenetic regulators of TMMs. Conversely, telomerase and ALT components influence cellular proliferation, mitochondrial function, glucose metabolism, and metabolic stress responses, not only in tumor cells but also in surrounding stromal and immune cells. This multidirectional cross-talk offers novel insights into tumor adaptability, immune evasion, and therapeutic opportunities.
This Special Issue aims to explore this emerging interface between telomere biology and cancer metabolism. We invite reviews and original research that dissect molecular links, identify therapeutic vulnerabilities, or profile metabolic-TMM interactions in diverse cancers. Contributions will help define how targeting this axis may unlock innovative strategies in precision oncology.
Dr. Ji-Yong Sung
Dr. Jiyue Zhu
Guest Editors
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Keywords
- telomere maintenance mechanisms (TMM)
- tumor microenvironment (TME)
- telomerase activation
- alternative lengthening of telomeres (ALT)
- cancer metabolism
- mitochondrial dysfunction
- redox homeostasis
- DNA damage response (DDR)
- epigenetic regulation
- cancer therapeutics
- senescence-associated secretory phenotypes (SASPs)
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