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Nathan Goodyear

DNA hypomethylation in cancer cells - 0 views

www.ncbi.nlm.nih.gov/...PMC2873040

cancer methylation hypomethylation

shared by Nathan Goodyear on 30 Jun 16 - No Cached
  • Nathan Goodyear on 30 Jun 16
     
    hypomethylation and carcinogenesis.
Nathan Goodyear

Acute Exercise Remodels Promoter Methylation in Human Skeletal Muscle: Cell Metabolism - 0 views

www.cell.com/...S1550-4131(12)00005-8

exercise methylation epigenetics muscle

shared by Nathan Goodyear on 03 Oct 17 - No Cached
  • our results provide evidence to suggest that acute exercise induces gene-specific DNA hypomethylation in human skeletal muscle
  • Our results suggest that DNA methylation is a component of the exercise-induced effect on expression of these genes.
  • Caffeine exposure decreased promoter methylation of Pgc-1α, Tfam, Mef2a, Cs, and Pdk4
  • ...4 more annotations...
  • the effect of exercise on DNA methylation in human skeletal muscle and provide evidence that acute exercise alters promoter methylation of exercise-responsive genes in a dose-dependent manner
  • DNA methylation was unaltered 48 hr after a 3-week exercise training program, whereas RNA expression of PGC-1α and TFAM promoters was elevated (data not shown), further suggesting that DNA hypomethylation is a transient mechanism involved in mRNA synthesis
  • Our findings that ionomycin, AICAR, or ROS production increased mRNA expression without altering promoter methylation may support the notion that DNA methylation does not exclusively control exercise-induced gene expression
  • acute exercise leads to transient changes in DNA methylation in adult skeletal muscle
  • Nathan Goodyear on 03 Oct 17
     
    Small study finds acute exercise is associated with epigenetic alteration of muscle through methylation.  This study found a hypomethylation of the genes PGC-1alpha, PDK4, and PPAR-delta with a respondent increase in expression.  The methylation activity was in the promoter region of these genes.
Nathan Goodyear

DNA methylation in cancer: too much, but also too little - 0 views

www.nature.com/...1205651a.html

cancer methylation hypermethylation hypomethylation

shared by Nathan Goodyear on 30 Jun 16 - No Cached
  • Nathan Goodyear on 30 Jun 16
     
    hypermethylation and hypomethylation shown to play roles in carcinogenesis.
Nathan Goodyear

S-Adenosylmethionine Inhibits the Growth of Cancer Cells by Reversing the Hypomethylati... - 0 views

www.ncbi.nlm.nih.gov/...PMC2999854

SAMe methylation oncogenes colon cancer cancer

shared by Nathan Goodyear on 27 Jun 12 - No Cached
  • Nathan Goodyear on 27 Jun 12
     
    SAMe shown to resolve the hypomethylation status of oncogenes. This allows increased genetic expression.  By improving methylation with SAMe, we can reduce oncogenic expression and thus be a useful cancer therapy adjunct.
Nathan Goodyear

The role of S-adenosyl methionine in preventing FOLFOX-induced liver toxicity: a retros... - 0 views

informahealthcare.com/...14740338.2011.562888

SAMe methylation cancer CBS cystathionine Beta-synthase glutathione GSH chemotherapy

shared by Nathan Goodyear on 27 Jun 12 - No Cached
  • Nathan Goodyear on 27 Jun 12
     
    SAMe shown to lower liver toxicity in chemotherapy treatment.  SAMe could be a powerful chemotherapeutic adjuvant.  This makes since, because cancer is known to be a hypomethylated state.  Low methyl donors will reduce CBS activity and thus lower glutathione.  This will result in increased oxidative stress and inflammation in the liver.  SAMe will open the CBS activity up and increase glutathione production.
Nathan Goodyear

Inhibitory effect of S-adenosylmethionine on the growth of human gastric cancer cells i... - 0 views

www.cjcsysu.cn/...752.pdf

SAMe cancer gastric cancer methylation

shared by Nathan Goodyear on 27 Jun 12 - No Cached
  • Nathan Goodyear on 27 Jun 12
     
    SAMe show a decrease in gastric cell growth in vitro and in vivo studies. This appears to be secondary to the resolved hypomethylation status of the c-myc and the uPA genes.
Nathan Goodyear

DNA methylation and cancer. - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...20920744

methylation hypermethylation hypomethylation cancer

shared by Nathan Goodyear on 30 Jun 16 - No Cached
  • Nathan Goodyear on 30 Jun 16
     
    hyper and hypo methylation known to be associated with carcinogenesis.  One carcinogenic potential of hypermethylation is through suppression of tumor suppression genes.
Nathan Goodyear

Abnormal transmethylation/transsulfuration metabolism and DNA hypomethylation among par... - 0 views

www.ncbi.nlm.nih.gov/...PMC2584168

autism spectrum disorders children detoxifcation methylation sulfation glutathione

shared by Nathan Goodyear on 05 Jul 11 - No Cached
  • Nathan Goodyear on 05 Jul 11
     
    abnormal detoxification at heart of autism
Nathan Goodyear

Curcumin Down-Regulates DNA Methyltransferase 1 and Plays an Anti-Leukemic Role in Acut... - 0 views

www.ncbi.nlm.nih.gov/...PMC3572185

aml acute myeloid leukemia cancer leukemia curcumin NF-kappaB

shared by Nathan Goodyear on 12 May 18 - No Cached
  • In a variety of solid tumors and blood cancers, aberrant hypermethylation of CpG-rich regions (>55% CG content, 0.5-4 kb in length, the so-called “CpG islands”) in the promoters of tumor suppressor genes (TSGs) results in their transcriptional silencing
  • These agents have been reported to suppress tumor growth by reversing aberrantly hypermethylation in the promoters of inactivated TSGs (e.g. p15INK4B), allowing re-expression of TSGs, thereby restoring normal cell cycle regulation, proliferation, apoptosis, and differentiation
  • groups have reported that curcumin acts as a scavenger of free radicals [13], an inhibitor of NF-κB nuclear translocation [14], and a modulator of histone deacetylase (HDAC) and histone acetyltransferase (HAT)
  • ...9 more annotations...
  • In this study, we found that curcumin down-regulated DNMT1 expression in AML cells. This occurred, at least in part, through down-modulation of two positive regulators of DNMT1: Sp1 and the NF-κB component, p65. We also found that curcumin-mediated down-regulation of DNMT1 was associated with reactivation of TSGs and tumor suppression, both in vivo and in vitro.
  • curcumin may selectively downregulate DNMT1 expression in tumor cells, but not in normal cells
  • DNMT1 expression is positively regulated by Sp1 and the NF-κB signaling component
  • indicating that curcumin may have significant anti-tumor activity in AML
  • We found that, compared to the vehicle control, curcumin treatment reduced tumor weight by 70%
  • Surprisingly, although curcumin significantly inhibited tumor growth in these mice, we were unable to find any obvious toxicity associated with curcumin treatment
  • Consistent with our observations regarding curcumin’s ability to inhibit tumor growth in vivo (Figure 4) and down-regulate DNMT1 expression in vitro and ex vivo (Figure 1), we found that decreased levels of DNMT1 protein and mRNA were expressed by tumor cells isolated from curcumin-treated mice
  • we identified curcumin as a substance which acts as an inhibitor of DNA methyltransferase enzymatic activity and induces significant global DNA hypomethylation in AML cells
  • In this study, we first demonstrated that curcumin decreases DNMT1 mRNA and protein expression levels, most likely through inhibiting expression of positive regulators of DNMT1, such as Sp1 and the p65 component of NF-κB component, and/or altering their ability to bind to the promoter region of DNMT1
  • Nathan Goodyear on 12 May 18
     
    Curcumin beneficial in AML
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