Body‐Wide Inactivation of the Myc‐Like Mlx Transcription Factor Network Accelerates Aging and Increases the Lifetime Cancer Incidence

Abstract The “Mlx” and “Myc” transcription factor networks cross‐communicate and share many common gene targets. Myc's activity depends upon its heterodimerization with Max, whereas the Mlx Network requires that the Max‐like factor Mlx associate with the Myc‐like factors MondoA or ChREBP. The c...

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Main Authors: Huabo Wang, Taylor Stevens, Jie Lu, Alexander Roberts, Clinton Van't Land, Radhika Muzumdar, Zhenwei Gong, Jerry Vockley, Edward V. Prochownik
Format: Article
Language:English
Published: Wiley 2024-09-01
Series:Advanced Science
Subjects:
Online Access:https://doi.org/10.1002/advs.202401593
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author Huabo Wang
Taylor Stevens
Jie Lu
Alexander Roberts
Clinton Van't Land
Radhika Muzumdar
Zhenwei Gong
Jerry Vockley
Edward V. Prochownik
author_facet Huabo Wang
Taylor Stevens
Jie Lu
Alexander Roberts
Clinton Van't Land
Radhika Muzumdar
Zhenwei Gong
Jerry Vockley
Edward V. Prochownik
author_sort Huabo Wang
collection DOAJ
description Abstract The “Mlx” and “Myc” transcription factor networks cross‐communicate and share many common gene targets. Myc's activity depends upon its heterodimerization with Max, whereas the Mlx Network requires that the Max‐like factor Mlx associate with the Myc‐like factors MondoA or ChREBP. The current work demonstrates that body‐wide Mlx inactivation, like that of Myc, accelerates numerous aging‐related phenotypes pertaining to body habitus and metabolism. The deregulation of numerous aging‐related Myc target gene sets is also accelerated. Among other functions, these gene sets often regulate ribosomal and mitochondrial structure and function, genomic stability, and aging. Whereas “MycKO” mice have an extended lifespan because of a lower cancer incidence, “MlxKO” mice have normal lifespans and a higher cancer incidence. Like Myc, the expression of Mlx, MondoA, and ChREBP and their control over their target genes deteriorate with age in both mice and humans. Collectively, these findings underscore the importance of lifelong and balanced cross‐talk between the two networks to maintain proper function and regulation of the many factors that can affect normal aging.
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spelling doaj-art-21d46c4a8a1c4ee19059c58c19da19c02025-08-20T01:55:19ZengWileyAdvanced Science2198-38442024-09-011134n/an/a10.1002/advs.202401593Body‐Wide Inactivation of the Myc‐Like Mlx Transcription Factor Network Accelerates Aging and Increases the Lifetime Cancer IncidenceHuabo Wang0Taylor Stevens1Jie Lu2Alexander Roberts3Clinton Van't Land4Radhika Muzumdar5Zhenwei Gong6Jerry Vockley7Edward V. Prochownik8Division of Hematology/Oncology UPMC Children's Hospital of Pittsburgh Pittsburgh PA 15201 USADivision of Hematology/Oncology UPMC Children's Hospital of Pittsburgh Pittsburgh PA 15201 USADivision of Hematology/Oncology UPMC Children's Hospital of Pittsburgh Pittsburgh PA 15201 USADivision of Hematology/Oncology UPMC Children's Hospital of Pittsburgh Pittsburgh PA 15201 USADivision of Medical Genetics UPMC Children's Hospital of Pittsburgh Pittsburgh PA 15201 USADivision of Endocrinology UPMC Children's Hospital of Pittsburgh Pittsburgh PA 15201 USADivision of Endocrinology UPMC Children's Hospital of Pittsburgh Pittsburgh PA 15201 USADivision of Medical Genetics UPMC Children's Hospital of Pittsburgh Pittsburgh PA 15201 USADivision of Hematology/Oncology UPMC Children's Hospital of Pittsburgh Pittsburgh PA 15201 USAAbstract The “Mlx” and “Myc” transcription factor networks cross‐communicate and share many common gene targets. Myc's activity depends upon its heterodimerization with Max, whereas the Mlx Network requires that the Max‐like factor Mlx associate with the Myc‐like factors MondoA or ChREBP. The current work demonstrates that body‐wide Mlx inactivation, like that of Myc, accelerates numerous aging‐related phenotypes pertaining to body habitus and metabolism. The deregulation of numerous aging‐related Myc target gene sets is also accelerated. Among other functions, these gene sets often regulate ribosomal and mitochondrial structure and function, genomic stability, and aging. Whereas “MycKO” mice have an extended lifespan because of a lower cancer incidence, “MlxKO” mice have normal lifespans and a higher cancer incidence. Like Myc, the expression of Mlx, MondoA, and ChREBP and their control over their target genes deteriorate with age in both mice and humans. Collectively, these findings underscore the importance of lifelong and balanced cross‐talk between the two networks to maintain proper function and regulation of the many factors that can affect normal aging.https://doi.org/10.1002/advs.202401593glycolysismitochondriareactive oxygen speciesTCA cycletelomeresWarburg effect
spellingShingle Huabo Wang
Taylor Stevens
Jie Lu
Alexander Roberts
Clinton Van't Land
Radhika Muzumdar
Zhenwei Gong
Jerry Vockley
Edward V. Prochownik
Body‐Wide Inactivation of the Myc‐Like Mlx Transcription Factor Network Accelerates Aging and Increases the Lifetime Cancer Incidence
Advanced Science
glycolysis
mitochondria
reactive oxygen species
TCA cycle
telomeres
Warburg effect
title Body‐Wide Inactivation of the Myc‐Like Mlx Transcription Factor Network Accelerates Aging and Increases the Lifetime Cancer Incidence
title_full Body‐Wide Inactivation of the Myc‐Like Mlx Transcription Factor Network Accelerates Aging and Increases the Lifetime Cancer Incidence
title_fullStr Body‐Wide Inactivation of the Myc‐Like Mlx Transcription Factor Network Accelerates Aging and Increases the Lifetime Cancer Incidence
title_full_unstemmed Body‐Wide Inactivation of the Myc‐Like Mlx Transcription Factor Network Accelerates Aging and Increases the Lifetime Cancer Incidence
title_short Body‐Wide Inactivation of the Myc‐Like Mlx Transcription Factor Network Accelerates Aging and Increases the Lifetime Cancer Incidence
title_sort body wide inactivation of the myc like mlx transcription factor network accelerates aging and increases the lifetime cancer incidence
topic glycolysis
mitochondria
reactive oxygen species
TCA cycle
telomeres
Warburg effect
url https://doi.org/10.1002/advs.202401593
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