The Contribution of Physiological and Accelerated Aging to Cancer Progression Through Senescence-Induced Inflammation

Morales-Valencia, Jorge; Gourichon, David

doi:10.3389/fonc.2021.747822

Cited by 9 publications

(4 citation statements)

References 99 publications

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“…SASP manifests as an inflammatory dysregulation observed in aged mammals and is associated with tumor initiation and progression. It contributes to the creation of a favorable TME or directly influences the intrinsic properties of tumor cells (Morales-Valencia and David, 2021). This revelation underscores the intricate relationship between aging, senescence, and cancer development, highlighting the dynamic and multifaceted nature of these processes.…”

Section: Senescencementioning

confidence: 87%

Inflammation and cancer: friend or foe?

Turizo-Smith,

Córdoba-Hernandez,

Mejía-Guarnizo

et al. 2024

Front. Pharmacol.

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Chronic inflammation plays a crucial role in the onset and progression of pathologies like neurodegenerative and cardiovascular diseases, diabetes, and cancer, since tumor development and chronic inflammation are linked, sharing common signaling pathways. At least 20% of breast and colorectal cancers are associated with chronic inflammation triggered by infections, irritants, or autoimmune diseases. Obesity, chronic inflammation, and cancer interconnection underscore the importance of population-based interventions in maintaining healthy body weight, to disrupt this axis. Given that the dietary inflammatory index is correlated with an increased risk of cancer, adopting an anti-inflammatory diet supplemented with nutraceuticals may be useful for cancer prevention. Natural products and their derivatives offer promising antitumor activity with favorable adverse effect profiles; however, the development of natural bioactive drugs is challenging due to their variability and complexity, requiring rigorous research processes. It has been shown that combining anti-inflammatory products, such as non-steroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and statins, with plant-derived products demonstrate clinical utility as accessible adjuvants to traditional therapeutic approaches, with known safety profiles. Pharmacological approaches targeting multiple proteins involved in inflammation and cancer pathogenesis emerge as a particularly promising option. Given the systemic and multifactorial nature of inflammation, comprehensive strategies are essential for long term success in cancer therapy. To gain insights into carcinogenic phenomena and discover diagnostic or clinically relevant biomarkers, is pivotal to understand genetic variability, environmental exposure, dietary habits, and TME composition, to establish therapeutic approaches based on molecular and genetic analysis. Furthermore, the use of endocannabinoid, cannabinoid, and prostamide-type compounds as potential therapeutic targets or biomarkers requires further investigation. This review aims to elucidate the role of specific etiological agents and mediators contributing to persistent inflammatory reactions in tumor development. It explores potential therapeutic strategies for cancer treatment, emphasizing the urgent need for cost-effective approaches to address cancer-associated inflammation.

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Section: Senescencementioning

confidence: 87%

Inflammation and cancer: friend or foe?

Turizo-Smith,

Córdoba-Hernandez,

Mejía-Guarnizo

et al. 2024

Front. Pharmacol.

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“…The accumulation of these factors alters the pathophysiology of cancer progression and may further accelerate the aging process. Senescent cells are scarce, but their SASP has powerful effects on in vivo tissue environments [ 39 ].…”

Section: Discussionmentioning

confidence: 99%

Senescence-associated exosomes transfer miRNA-induced fibrosis to neighboring cells

Lee

Ghosh

Koh

et al. 2023

Aging

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Radiation-induced fibrosis is a common side effect of radiotherapy, which is the most common treatment for cancer. However, radiation also causes p53-mediated cell cycle arrest, prolonged expression of p21, and the development of senescence in normal cells that reside in irradiated tissues. Bone marrow-derived mesenchymal stem cells (MSCs) accumulate in primary tumor sites because of their natural tropism for inflammatory and fibrotic tissues. MSCs are extremely sensitive to low doses of ionizing radiation and acquire senescence as a result of bystander radiation effects. Senescent cells remain metabolically active but develop a potent senescence-associated secretory phenotype (SASP) that correlates to hyperactive secretion of cytokines, pro-fibrotic growth factors, and exosomes (EXOs). Integrative pathway analysis highlighted that radiationinduced senescence significantly enriched cell-cycle, extracellular matrix, transforming growth factor-β (TGF-β) signaling, and vesicle-mediated transport genes in MSCs. EXOs are cell-secreted nanovesicles (a subclass of small extracellular vesicles) that contain biomaterials-proteins, RNAs, microRNAs (miRNAs)-that are critical in cell-cell communication. miRNA content analysis of secreted EXOs further revealed that radiation-induced senescence uniquely altered miRNA profiles. In fact, several of the standout miRNAs directly targeted TGF-β or downstream genes. To examine bystander effects of radiation-induced senescence, we further treated normal MSCs with senescence-associated EXOs (SA-EXOs). These modulated genes related to TGF-β pathway and elevated both alpha smooth muscle actin (protein increased in senescent, activated cells) and Ki-67 (proliferative marker) expression in SA-EXO treated MSCs compared to untreated MSCs. We revealed SA-EXOs possess unique miRNA content that influence myofibroblast phenotypes via TGF-β pathway activation. This highlights that SA-EXOs are potent SASP factors that play a large role in cancer-related fibrosis.

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“…In animal models, interventions and genetic manipulations that delay aging and extend lifespan, such as caloric restriction, have been shown to exert significant anti-cancer effects [267][268][269][270][271][272][273][274]. Conversely, interventions and genetic manipulations that accelerate aging and shorten lifespan promote tumorigenesis and cancer progression [275][276][277].…”

Section: Malignant Diseasesmentioning

confidence: 99%

Exposome and unhealthy aging: environmental drivers from air pollution to occupational exposures

Pandics,

Major,

Fazekas-Pongor

et al. 2023

GeroScience

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The aging population worldwide is facing a significant increase in age-related non-communicable diseases, including cardiovascular and brain pathologies. This comprehensive review paper delves into the impact of the exposome, which encompasses the totality of environmental exposures, on unhealthy aging. It explores how environmental factors contribute to the acceleration of aging processes, increase biological age, and facilitate the development and progression of a wide range of age-associated diseases. The impact of environmental factors on cognitive health and the development of chronic age-related diseases affecting the cardiovascular system and central nervous system is discussed, with a specific focus on Alzheimer’s disease, Parkinson’s disease, stroke, small vessel disease, and vascular cognitive impairment (VCI). Aging is a major risk factor for these diseases. Their pathogenesis involves cellular and molecular mechanisms of aging such as increased oxidative stress, impaired mitochondrial function, DNA damage, and inflammation and is influenced by environmental factors. Environmental toxicants, including ambient particulate matter, pesticides, heavy metals, and organic solvents, have been identified as significant contributors to cardiovascular and brain aging disorders. These toxicants can inflict both macro- and microvascular damage and many of them can also cross the blood–brain barrier, inducing neurotoxic effects, neuroinflammation, and neuronal dysfunction. In conclusion, environmental factors play a critical role in modulating cardiovascular and brain aging. A deeper understanding of how environmental toxicants exacerbate aging processes and contribute to the pathogenesis of neurodegenerative diseases, VCI, and dementia is crucial for the development of preventive strategies and interventions to promote cardiovascular, cerebrovascular, and brain health. By mitigating exposure to harmful environmental factors and promoting healthy aging, we can strive to reduce the burden of age-related cardiovascular and brain pathologies in the aging population.

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The Contribution of Physiological and Accelerated Aging to Cancer Progression Through Senescence-Induced Inflammation

Cited by 9 publications

References 99 publications

Inflammation and cancer: friend or foe?

Inflammation and cancer: friend or foe?

Senescence-associated exosomes transfer miRNA-induced fibrosis to neighboring cells

Exposome and unhealthy aging: environmental drivers from air pollution to occupational exposures

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