ArticleThe Prostate2012
Activation of silenced tumor suppressor genes in prostate cancer cells by a novel energy restriction-mimetic agent.
Article in The Prostate, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 24 citations in OpenAlex.
- Review
- Cellular metabolism regulates the differentiation and function of T-cell subsets.Cellular & molecular immunology · 2024Review
- Coexpression Network Analysis of lncRNA Associated with Overexpression of DNMT1 in Esophageal Epithelial Cells.BioMed research international · 2021Article
- Identification of key DNA methylation-driven genes in prostate adenocarcinoma: an integrative analysis of TCGA methylation data.Journal of translational medicine · 2019Article
- Targeting T Cell Activation and Lupus Autoimmune Phenotypes by Inhibiting Glucose Transporters.Frontiers in immunology · 2019Article
- Current Stem Cell Biomarkers and Their Functional Mechanisms in Prostate Cancer.International journal of molecular sciences · 2016Review
- Restoration of Brain Acid Soluble Protein 1 Inhibits Proliferation and Migration of Thyroid Cancer Cells.Chinese medical journal · 2016Article
- Does Wnt/β-catenin pathway contribute to the stability of DNMT1 expression in urological cancer cell lines?Experimental biology and medicine (Maywood, N.J.) · 2015Article
- HIGD1A Regulates Oxygen Consumption, ROS Production, and AMPK Activity during Glucose Deprivation to Modulate Cell Survival and Tumor Growth.Cell reports · 2015Article
- Albumin-induced apoptosis of tubular cells is modulated by BASP1.Cell death & disease · 2015Article
- Role of DNA methyltransferase 1 on the altered eNOS expression in human umbilical endothelium from intrauterine growth restricted fetuses.Epigenetics · 2013Article
- Suppression of prostate epithelial proliferation and intraprostatic progrowth signaling in transgenic mice by a new energy restriction-mimetic agent.Cancer prevention research (Philadelphia, Pa.) · 2013Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundTargeting tumor metabolism by energy restriction-mimetic agents (ERMAs) has emerged as a strategy for cancer therapy/prevention. Evidence suggests a mechanistic link between ERMA-mediated antitumor effects and epigenetic gene regulation.
methodsMicroarray analysis showed that a novel thiazolidinedione-derived ERMA, CG-12, and glucose deprivation could suppress DNA methyltransferase (DNMT)1 expression and reactivate DNA methylation-silenced tumor suppressor genes in LNCaP prostate cancer cells. Thus, we investigated the effects of a potent CG-12 derivative, CG-5, vis-à-vis 2-deoxyglucose, glucose deprivation and/or 5-aza-deoxycytidine, on DNMT isoform expression (Western blotting, RT-PCR), DNMT1 transcriptional activation (luciferase reporter assay), and expression of genes frequently hypermethylated in prostate cancer (quantitative real-time PCR). Promoter methylation was assessed by pyrosequencing analysis. SiRNA-mediated knockdown and ectopic expression of DNMT1 were used to validate DNMT1 as a target of CG-5.
resultsCG-5 and glucose deprivation upregulated the expression of DNA methylation-silenced tumor suppressor genes, including GADD45a, GADD45b, IGFBP3, LAMB3, BASP1, GPX3, and GSTP1, but also downregulated methylated tumor/invasion-promoting genes, including CD44, S100A4, and TACSTD2. In contrast, 5-aza-deoxycytidine induced global reactivation of these genes. CG-5 mediated these epigenetic effects by transcriptional repression of DNMT1, which was associated with reduced expression of Sp1 and E2F1. SiRNA-mediated knockdown and ectopic expression of DNMT1 corroborated DNMT1's role in the modulation of gene expression by CG-5. Pyrosequencing revealed differential effects of CG-5 versus 5-aza-deoxycytidine on promoter methylation in these genes.
conclusionsThese findings reveal a previously uncharacterized epigenetic effect of ERMAs on DNA methylation-silenced tumor suppressor genes, which may foster novel strategies for prostate cancer therapy.
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