Common gene signature of cancer and longevity

Budovsky, Arie; Tăcutu, Robi; Yanai, Hagai; Abramovich, Amir; Wolfson, Marina; Fraifeld, Vadim E.

doi:10.1016/j.mad.2008.04.002

Cited by 51 publications

(39 citation statements)

References 60 publications

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“…We have taken this gap into account, and intend to expand our database accordingly in our future builds. Yet, the merit of using criteria based only on direct interventions, has been previously shown for the analysis of complex phenomena such as aging, age-related diseases, and cellular senescence [19, 24, 36]. …”

Section: Discussionmentioning

confidence: 99%

Tissue repair genes: the TiRe database and its implication for skin wound healing

et al. 2016

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Wound healing is an inherent feature of any multicellular organism and recent years have brought about a huge amount of data regarding regular and abnormal tissue repair. Despite the accumulated knowledge, modulation of wound healing is still a major biomedical challenge, especially in advanced ages. In order to collect and systematically organize what we know about the key players in wound healing, we created the TiRe (Tissue Repair) database, an online collection of genes and proteins that were shown to directly affect skin wound healing. To date, TiRe contains 397 entries for four organisms: Mus musculus, Rattus norvegicus, Sus domesticus, and Homo sapiens. Analysis of the TiRe dataset of skin wound healing-associated genes showed that skin wound healing genes are (i) over-conserved among vertebrates, but are under-conserved in invertebrates; (ii) enriched in extracellular and immuno-inflammatory genes; and display (iii) high interconnectivity and connectivity to other proteins. The latter may provide potential therapeutic targets. In addition, a slower or faster skin wound healing is indicative of an aging or longevity phenotype only when assessed in advanced ages, but not in the young. In the long run, we aim for TiRe to be a one-station resource that provides researchers and clinicians with the essential data needed for a better understanding of the mechanisms of wound healing, designing new experiments, and the development of new therapeutic strategies. TiRe is freely available online at http://www.tiredb.org.

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Section: Discussionmentioning

confidence: 99%

Tissue repair genes: the TiRe database and its implication for skin wound healing

et al. 2016

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“…It should be noted that the relationship between aging-associated chronic diseases and development has been recently described by means of network analyses (Budovsky et al 2009). In this sense, a comparison of the common signature of longevity and age-related disease proteins (ARDs) network present in the NetAge database (Tacutu et al 2010) and described in the manuscript of Budovsky et al (2009), with the PPPI network of H. sapiens, indicated the presence of 57 common proteins, all participating in epigenetic mechanism, development, and aging.…”

Section: A Model Linking Devage With Dohad In An Antagonistic Pleiotrmentioning

confidence: 99%

The developmental aging and origins of health and disease hypotheses explained by different protein networks

2011

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One theory that attempts to explain how and why an organism ages is the developmental hypothesis of aging (DevAge), which describes how developmental programming leads to aging in adults. Interestingly, the developmental origins of health and disease hypothesis (DOHaD) asserts that some aging-associated diseases that occur in adults are closely related to development and to conditions in the intrauterine environment. Thus, both aging and aging-associated diseases can be viewed, at least in part, as the result of a developmental program that is activated early in embryogenesis and persists throughout the lifespan of the organism. We would expect this developmental program to be regulated by a set of interacting protein networks that connect environmental and molecular signals. However, the connection between aging and development is not clear. Thus, a systems biology approach that incorporates different "omic" databases for two mammalian models, Homo sapiens and Mus musculus, was used to evaluate how development and aging are interconnected. Interestingly, three major, evolutionarily conserved processes, namely the immune system, epigenetics, and aerobic metabolism, appear to regulate aging and development in both H. sapiens and M. musculus. Considering that these three processes are essential to embryogenesis, the protein networks within these processes are subjected to strong selective pressure to eliminate gross developmental abnormalities in early embryogenesis. This selective pressure becomes more relaxed in the adult organism, permitting the onset of aging-associated diseases and inflammation-related aging; this concept echoes the antagonistic pleiotropy hypothesis of aging.

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“…Given a common molecular basis of aging and ARDs (Blagosklonny 2008;Budovsky et al 2009;Tacutu et al 2010;Wolfson et al 2009), getting insight into the role of cell polarity in ARDs would also shed light on its role in the mechanisms of aging. Both direct and indirect evidence suggests that disruption of cell polarity is implicated in the development of major ARDs such as Alzheimer's disease (Aronov et al 1999(Aronov et al , 2001Brandt 2001; Matenia and Mandelkow Compared to other ARDs, the disruption of cell polarity is mostly studied in cancer.…”

Section: Human Cellsmentioning

confidence: 99%

Linking cell polarity, aging and rejuvenation

2010

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Cell polarity is a universal biological phenomenon. While much is known about the establishment and maintenance of cell polarity, its role in aging and age-related diseases remains to be fully addressed. Nonetheless, the exciting findings in the budding yeast indicate that the polar processes are intimately linked to both aging of the mother cell and rejuvenation of the daughter cell. This includes polar segregation of damaged proteins and ERCs due to the septin-based diffusion barrier, asymmetric inheritance of MDR proteins and retrograde protein transport. The principal, still unexplored question is whether the same polar mechanisms work during the asymmetric division of germ and stem cells, allowing their rejuvenation across generations. Further strengthening the links between cell polarity and aging is a large number of common genes associated with both polarity and longevity. Given a strong similarity between mechanisms of cell polarity in yeast and higher eukaryotes, the budding yeast Saccharomyces cerevisiae could serve as a convenient model system for studying the links between the cell polarity, aging and rejuvenation. Consequently, exploring the potential mammalian equivalents of yeast-established polarity mechanisms could be the focus for future biogerontological investigations.

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Common gene signature of cancer and longevity

Cited by 51 publications

References 60 publications

Tissue repair genes: the TiRe database and its implication for skin wound healing

Tissue repair genes: the TiRe database and its implication for skin wound healing

The developmental aging and origins of health and disease hypotheses explained by different protein networks

Linking cell polarity, aging and rejuvenation

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