Unveiling the Relation between Cellular Aging, Epigenetics and Cancer

This Editorial article intends to unravel the relationships among cellular aging, epigenetic changes, and tumorigenesis, thereby offering perspectives that could improve therapeutic approaches in cancer management and promote future research on these topics. Furthermore, selected fundamental principles concerning cellular aging will be presented to elucidate how this process contributes to the comprehension of tumorigenesis. As humans age, there is a progressive decline in physiological functions, which significantly increases the risk of cancer. Epigenetic alterations-heritable yet reversible modifications of the genome without changes in DNA sequence-play a pivotal role in both aging and tumorigenesis. Age-associated epigenetic drift, involving widespread DNA methylation changes, histone modification shifts, and chromatin remodelling, disrupts normal gene regulatory networks, leading to genomic instability and impaired cellular homeostasis. Additionally, the accumulation of senescent cells, driven by epigenetic dysregulation, fosters a pro-inflammatory environment that can promote tumorigenesis. Moreover, the epigenetic landscape of aged tissues resembles that of cancerous tissues, suggesting that aging establishes a permissive environment for malignant transformation. Understanding the interplay between aging, epigenetic regulation, and cancer is critical for the development of preventive strategies and novel therapeutics. Epigenetic reprogramming technologies, aiming to restore youthful epigenetic states, hold promise for delaying aging and reducing cancer incidence. However, challenges remain in selectively targeting pathogenic epigenetic changes without disrupting essential cellular functions.