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Matti Narkia

Glucose restriction can extend normal cell lifespan and impair precancerous cell growth... - 0 views

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    Glucose restriction can extend normal cell lifespan and impair precancerous cell growth through epigenetic control of hTERT and p16 expression.
    Li Y, Liu L, Tollefsbol TO.
    FASEB J. 2009 Dec 17. [Epub ahead of print]
    PMID: 20019239
    doi: 10.1096/fj.09-149328

    Cancer cells metabolize glucose at elevated rates and have a higher sensitivity to glucose reduction. However, the precise molecular mechanisms leading to different responses to glucose restriction between normal and cancer cells are not fully understood. We analyzed normal WI-38 and immortalized WI-38/S fetal lung fibroblasts and found that glucose restriction resulted in growth inhibition and apoptosis in WI-38/S cells, whereas it induced lifespan extension in WI-38 cells. Moreover, in WI-38/S cells glucose restriction decreased expression of hTERT (human telomerase reverse transcriptase) and increased expression of p16(INK4a). Opposite effects were found in the gene expression of hTERT and p16 in WI-38 cells in response to glucose restriction. The altered gene expression was partly due to glucose restriction-induced DNA methylation changes and chromatin remodeling of the hTERT and p16 promoters in normal and immortalized WI-38 cells. Furthermore, glucose restriction resulted in altered hTERT and p16 expression in response to epigenetic regulators in WI-38 rather than WI-38/S cells, suggesting that energy stress-induced differential epigenetic regulation may lead to different cellular fates in normal and precancerous cells. Collectively, these results provide new insights into the epigenetic mechanisms of a nutrient control strategy that may contribute to cancer therapy as well as antiaging approaches.
Matti Narkia

Calorie restriction: Scientists take important step toward 'fountain of youth' - 0 views

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    "ScienceDaily (Dec. 26, 2009) - Going back for a second dessert after your holiday meal might not be the best strategy for living a long, cancer-free life say researchers from the University of Alabama at Birmingham. That's because they've shown exactly how restricted calorie diets -- specifically in the form of restricted glucose -- help human cells live longer.


    They found that the normal cells lived longer, and many of the precancerous cells died, when given less glucose. Gene activity was also measured under these same conditions. The reduced glucose caused normal cells to have a higher activity of the gene that dictates the level of telomerase, an enzyme that extends their lifespan and lower activity of a gene (p16) that slows their growth. Epigenetic effects (effects not due to gene mutations) were found to be a major cause in changing the activity of these genes as they reacted to decreased glucose levels.

    "Western science is on the cusp of developing a pharmaceutical fountain of youth" said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal. "This study confirms that we are on the path to persuading human cells to let us to live longer, and perhaps cancer-free, lives.""
Matti Narkia

Researchers link calorie intake to cell lifespan, cancer development (w/ Video) - 0 views

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    "Researchers from the University of Alabama at Birmingham (UAB) have discovered that restricting consumption of glucose, the most common dietary sugar, can extend the life of healthy human-lung cells and speed the death of precancerous human-lung cells, reducing cancer's spread and growth rate.

    The research has wide-ranging potential in age-related science, including ways in which calorie-intake restriction can benefit longevity and help prevent diseases like cancer that have been linked to aging, said principal investigator Trygve Tollefsbol, Ph.D., D.O., a professor in the Department of Biology.

    "These results further verify the potential health benefits of controlling calorie intake." Tollefsbol said. "Our research indicates that calorie reduction extends the lifespan of healthy human cells and aids the body's natural ability to kill off cancer-forming cells.
Matti Narkia

Calorie intake linked to cell lifespan, cancer development - 0 views

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    "ScienceDaily (Dec. 17, 2009) - Researchers from the University of Alabama at Birmingham (UAB) have discovered that restricting consumption of glucose, the most common dietary sugar, can extend the life of healthy human-lung cells and speed the death of precancerous human-lung cells, reducing cancer's spread and growth rate.

    The research has wide-ranging potential in age-related science, including ways in which calorie-intake restriction can benefit longevity and help prevent diseases like cancer that have been linked to aging, said principal investigator Trygve Tollefsbol, Ph.D., D.O., a professor in the Department of Biology.

    "These results further verify the potential health benefits of controlling calorie intake." Tollefsbol said. "Our research indicates that calorie reduction extends the lifespan of healthy human cells and aids the body's natural ability to kill off cancer-forming cells.""
Matti Narkia

Vitamin D and aging. [J Steroid Biochem Mol Biol. 2009] - PubMed result - 0 views

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    Vitamin D and aging.
    Tuohimaa P.
    J Steroid Biochem Mol Biol. 2009 Mar;114(1-2):78-84. Review.
    PMID: 19444937
Matti Narkia

Induction of Ovarian Cancer Cell Apoptosis by 1,25-Dihydroxyvitamin D3 through the Down... - 0 views

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    Induction of ovarian cancer cell apoptosis by 1,25-dihydroxyvitamin D3 through the down-regulation of telomerase.
    Jiang F, Bao J, Li P, Nicosia SV, Bai W.
    J Biol Chem. 2004 Dec 17;279(51):53213-21. Epub 2004 Oct 12.
    PMID: 15485861
    doi: 10.1074/jbc.M410395200

    Overall, the study suggests that the down-regulation of telomerase activity by 1,25(OH)2VD3 and the resulting cell death are important components of the response of OCa cells to 1,25(OH)2VD3-induced growth suppression.

    Progressive shortening of telomere associated with cell divisions limits the life span of normal cells and eventually leads to senescence. To become immortal, human cancers including OCa are invariably associated with activation of mechanism that maintains telomere length. Approximately 85-90% of cancers show reactivation of telomerase. The present study shows that telomerase in OCa cells is down-regulated by 1,25(OH)2VD3. Down-regulation of telomerase is due to decreased stability of hTERT mRNA rather than VDRE-mediated transcriptional repression through the putative VDRE present in the regulatory region of the hTERT gene.

    It is known that the inhibition of telomerase may lead to a phenotypic lag during which cells would continue to divide until the point at which the telomeres became critically short. This phenomenon may explain why the apoptotic induction by 1,25(OH)2VD3 needs the treatment for more than 6 days. As mentioned in the results, no detectable shortening of telomeric repeats was observed in parental OVCAR3 cells after 9 days of treatment with 1,25(OH)2VD3 (Fig. 4D). This is likely due to the fact that the short telomere (about 3 kb) in OVCAR3 cells is very close to the minimal length required for survival and that cells with detectably shorter telomere may have been selected against apoptosis. It has been shown that transformed human cells enter crisis once the terminal restriction fragment of the telomere reaches a length of about 4 kb. This is insufficient to protect chro
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