Common Pathogenetic Mechanisms Underlying Aging and Tumor and Means of Interventions

Abstract

Recently, there has been an increase in the incidence of malignant tumors among the older population. Moreover, there is an association between aging and cancer. During the process of senescence, the human body suffers from a series of imbalances, which have been shown to further accelerate aging, trigger tumorigenesis, and facilitate cancer progression. Therefore, exploring the junctions of aging and cancer and searching for novel methods to restore the junctions is of great importance to intervene against aging-related cancers. In this review, we have identified the underlying pathogenetic mechanisms of aging-related cancers by comparing alterations in the human body caused by aging and the factors that trigger cancers. We found that the common mechanisms of aging and cancer include cellular senescence, alterations in proteostasis, microbiota disorders (decreased probiotics and increased pernicious bacteria), persistent chronic inflammation, extensive immunosenescence, inordinate energy metabolism, altered material metabolism, endocrine disorders, altered genetic expression, and epigenetic modification. Furthermore, we have proposed that aging and cancer have common means of intervention, including novel uses of common medicine (metformin, resveratrol, and rapamycin), dietary restriction, and artificial microbiota intervention or selectively replenishing scarce metabolites. In addition, we have summarized the research progress of each intervention and revealed their bidirectional effects on cancer progression to compare their reliability and feasibility. Therefore, the study findings provide vital information for advanced research studies on age-related cancers. However, there is a need for further optimization of the described methods and more suitable methods for complicated clinical practices. In conclusion, targeting aging may have potential therapeutic effects on aging-related cancers.

Pan-cancer analysis of RNA 5-methylcytosine reader (ALYREF)

“…Recent studies indicate that aging is accompanied by progressive epigenetic alterations in both dividing and nondividing cells [55], with epigenetic changes proposed as a hallmark of aging by 2023 [56]. Aging is a risk factor for various age-related diseases, including cancers [57][58][59][60] and degenerative diseases [61][62][63][64]. Our study found that ALYREF expression was significantly related to aging, confirming the link between epigenomics, aging, and cancer.…”

SKA3 targeted therapies in cancer precision surgery: bridging bench discoveries to clinical applications – review article

“…These included: (1) molecular biomarker for preoperative evaluation: surgeons can further assess the practical value of SKA3 as a molecular biomarker before surgery, exploring its potential as a predictive indicator for patient prognosis and surgical selection; (2) practical impact on surgical outcomes: surgeons can conduct a more in-depth analysis of how SKA3 overexpression affects surgical outcomes, such as postoperative survival, tumor clearance, and postsurgery monitoring, which might contributed to establishing a direct link between research findings and practical implications in surgical practice; (3) clinical application prospects: in the future, surgeons might improve patient prognosis through therapeutic interventions targeting SKA3 and the practical prospects of implementing these interventions in surgical treatments. In addition, the relationship between aging and cancer susceptibility has been extensively documented, with older individuals demonstrating a higher likelihood of developing malignant tumors compared to their younger counterparts 105 – 110 . As the global population ages, a surge in cancer incidence is projected over the next few decades 102 , 111 .…”

A new perspective on prostate cancer treatment: the interplay between cellular senescence and treatment resistance

“…Exposure of PCa to therapies targeting AR, different anticancer compounds, and ionizing radiation can induce a senescent phenotype, termed therapy-induced senescence (TIS) ( 65 ). The shared mechanisms of senescence and PCa encompass disruptions in proteostasis, dysbiosis of the microbiota, persistent chronic inflammation, and widespread immunosenescence ( 66 ). TIS may benefit patients in the treatment of PCa ( 67 ).…”