Start Date
April 2024
Location
2nd floor - Library
Abstract
The regulation of RNA polymerase III by MAF1 is crucial for cellular homeostasis. Its disruption is linked to accelerated aging and an increased risk of age-related cancers. This research identifies and analyzes significant mutations in MAF1, which lead to overactive Pol III, suggesting these mutations as critical biomarkers for assessing aging processes and cancer susceptibility. MAF1 mutations related to cancer are most often seen as cancer in the large intestine, primarily affecting individuals aged 71-80. Most MAF1 mutations associated with cancer were mutations of coding regions, underlining their potential impact on protein function and cellular processes. Leveraging the Catalog of Somatic Mutations in Cancer (COSMIC), we extracted relevant MAF1 mutation data. Subsequently, we employed the Cancer-Related Analysis of Variants Toolkit (CRAVAT) for an in-depth evaluation of these mutations' potential impact on aging and cancer risk. Computational modeling identified specific MAF1 mutations that pose a high risk of enhancing Pol III activity, thus potentially accelerating the aging process and increasing the susceptibility to age-related cancers. We hypothesize that if an identified single nucleotide polymorphism (SNP) damages the shape and function of the MAF1 protein, it could lead to a decrease in its regulatory function. This decrease in function may subsequently increase Pol III transcription. Increased transcription can cause cellular stress and metabolic imbalance, contributing to a shorter lifespan. The results offer new perspectives on the genetic foundations of aging and propose that focusing on MAF1 and specific SNP mutations could open up innovative therapeutic strategies for slowing down the aging process and averting associated cancers. This study advances our understanding of the genetic factors contributing to aging and also opens up possibilities for developing targeted interventions aimed at mitigating the risk of age-associated diseases.
Unraveling the Role of MAF1 Mutations in Accelerating Aging
2nd floor - Library
The regulation of RNA polymerase III by MAF1 is crucial for cellular homeostasis. Its disruption is linked to accelerated aging and an increased risk of age-related cancers. This research identifies and analyzes significant mutations in MAF1, which lead to overactive Pol III, suggesting these mutations as critical biomarkers for assessing aging processes and cancer susceptibility. MAF1 mutations related to cancer are most often seen as cancer in the large intestine, primarily affecting individuals aged 71-80. Most MAF1 mutations associated with cancer were mutations of coding regions, underlining their potential impact on protein function and cellular processes. Leveraging the Catalog of Somatic Mutations in Cancer (COSMIC), we extracted relevant MAF1 mutation data. Subsequently, we employed the Cancer-Related Analysis of Variants Toolkit (CRAVAT) for an in-depth evaluation of these mutations' potential impact on aging and cancer risk. Computational modeling identified specific MAF1 mutations that pose a high risk of enhancing Pol III activity, thus potentially accelerating the aging process and increasing the susceptibility to age-related cancers. We hypothesize that if an identified single nucleotide polymorphism (SNP) damages the shape and function of the MAF1 protein, it could lead to a decrease in its regulatory function. This decrease in function may subsequently increase Pol III transcription. Increased transcription can cause cellular stress and metabolic imbalance, contributing to a shorter lifespan. The results offer new perspectives on the genetic foundations of aging and propose that focusing on MAF1 and specific SNP mutations could open up innovative therapeutic strategies for slowing down the aging process and averting associated cancers. This study advances our understanding of the genetic factors contributing to aging and also opens up possibilities for developing targeted interventions aimed at mitigating the risk of age-associated diseases.
