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1. Full Text Genistein mediated histone acetylation and demethylation activates tumor suppressor genes in prostate cancer cells
by Kikuno, Nobuyuki and Shiina, Hiroaki and Urakami, Shinji and Kawamoto, Ken and Hirata, Hiroshi and Tanaka, Yuichiro and Majid, Shahana and Igawa, Mikio and Dahiya, Rajvir
International Journal of Cancer, ISSN 0020-7136, 08/2008, Volume 123, Issue 3, pp. 552 - 560
Genistein is a phytoestrogen that has been reported to suppress the AKT signaling pathway in several malignancies. However, the molecular mechanism of... 
Prostate cancer | Genistein | Tumor suppressor gene | APOPTOSIS | METHYLATION | PROTEIN-KINASE | TRANSCRIPTION | SIRT1 | FACULTATIVE HETEROCHROMATIN | CYLD | prostate cancer | genistein | ONCOLOGY | SIGNALING PATHWAY | NF-KAPPA-B | EXPRESSION | tumor suppressor gene | PTEN Phosphohydrolase - drug effects | Prostatic Neoplasms - metabolism | Deubiquitinating Enzyme CYLD | CpG Islands - drug effects | Humans | Male | NF-kappa B - metabolism | Phosphatidylinositol 3-Kinases - metabolism | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Genes, Tumor Suppressor - drug effects | Genes, p53 - drug effects | Prostatic Neoplasms - genetics | Chromatin Immunoprecipitation | Forkhead Transcription Factors - metabolism | Sirtuin 1 | Antimetabolites, Antineoplastic - pharmacology | Electrophoretic Mobility Shift Assay | Gene Expression Regulation, Neoplastic - drug effects | Chromones - pharmacology | Anticarcinogenic Agents - pharmacology | Hydroxamic Acids - pharmacology | Phytoestrogens - pharmacology | Prostatic Neoplasms - drug therapy | PTEN Phosphohydrolase - genetics | Tumor Suppressor Proteins - metabolism | Enzyme Inhibitors - pharmacology | Morpholines - pharmacology | PTEN Phosphohydrolase - metabolism | Azacitidine - analogs & derivatives | Down-Regulation - drug effects | Reverse Transcriptase Polymerase Chain Reaction | Blotting, Western | Histones - drug effects | Gene Expression Regulation - drug effects | Up-Regulation - drug effects | Azacitidine - pharmacology | Acetylation - drug effects | Methylation - drug effects | Genistein - pharmacology | Cell Line, Tumor | Protein Kinase Inhibitors - pharmacology | Histones - metabolism | Forkhead Box Protein O3 | Sirtuins - metabolism | NF-kappa B - drug effects | Index Medicus
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2. Full Text Targeting calcium signaling induces epigenetic reactivation of tumor suppressor genes in cancer
by Raynal, Noël J.-M and Lee, Justin T and Wang, Youjun and Beaudry, Annie and Madireddi, Priyanka and Garriga, Judith and Malouf, Gabriel G and Dumont, Sarah and Dettman, Elisha J and Gharibyan, Vazganush and Ahmed, Saira and Chung, Woonbok and Childers, Wayne E and Abou-Gharbia, Magid and Henry, Ryan A and Andrews, Andrew J and Jelinek, Jaroslav and Cui, Ying and Baylin, Stephen B and Gill, Donald L and Issa, Jean-Pierre J
Cancer Research, ISSN 0008-5472, 03/2016, Volume 76, Issue 6, pp. 1494 - 1505
Targeting epigenetic pathways is a promising approach for cancer therapy. Here, we report on the unexpected finding that targeting calcium signaling can... 
Colonic Neoplasms - genetics | Gene Silencing - drug effects | Calcium - metabolism | CpG Islands - drug effects | Colonic Neoplasms - drug therapy | Humans | Promoter Regions, Genetic - drug effects | Promoter Regions, Genetic - genetics | Genes, Tumor Suppressor - drug effects | Epigenomics - methods | HEK293 Cells | Antineoplastic Agents - pharmacology | Epigenesis, Genetic - drug effects | Gene Expression Regulation, Neoplastic - drug effects | Nuclear Proteins - genetics | Gene Expression Regulation, Neoplastic - genetics | Cell Line | HCT116 Cells | DNA Methylation - genetics | Signal Transduction - genetics | Signal Transduction - drug effects | Calcium Signaling - drug effects | Epigenesis, Genetic - genetics | K562 Cells | Cell Line, Tumor | CpG Islands - genetics | HL-60 Cells | Histone Deacetylase Inhibitors - pharmacology | Calcium Signaling - genetics | DNA Methylation - drug effects
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3. Full Text The tobacco-specific carcinogen NNK induces DNA methyltransferase 1 accumulation and tumor suppressor gene hypermethylation in mice and lung cancer patients
by Lin, Ruo-Kai and Hsieh, Yi-Shuan and Lin, Pinpin and Hsu, Han-Shui and Chen, Chih-Yi and Tang, Yen-An and Lee, Chung-Fan and Wang, Yi-Ching
Journal of Clinical Investigation, ISSN 0021-9738, 02/2010, Volume 120, Issue 2, pp. 521 - 532
DNA methyltransferase 1 (DNMT1) catalyzes DNA methylation and is overexpressed in many human diseases, including cancer. The tobacco-specific carcinogen NNK... 
AIRWAY EPITHELIAL-CELLS | PATHWAYS | MEDICINE, RESEARCH & EXPERIMENTAL | PROMOTER HYPERMETHYLATION | METHYLATION | EPIGENETICS | PROTEIN | NICOTINE | PROGNOSIS | CIGARETTE-SMOKE | EXPRESSION | Smoking - adverse effects | Cell Line | Phosphorylation | Lung Neoplasms - enzymology | Prognosis | DNA (Cytosine-5-)-Methyltransferase 1 | Humans | Nitrosamines - toxicity | Carcinogens - toxicity | Genes, Tumor Suppressor - drug effects | Animals | Cell Line, Tumor | DNA (Cytosine-5-)-Methyltransferases - drug effects | Mice | DNA Methylation - drug effects | DNA (Cytosine-5-)-Methyltransferases - biosynthesis | Carcinogens | Lung cancer | Cocarcinogens | Physiological aspects | Development and progression | Genetic aspects | Research | Methylation | Health aspects | Smoking | Cancer
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4. Full Text Decitabine and suberoylanilide hydroxamic acid (SAHA) inhibit growth of ovarian cancer cell lines and xenografts while inducing expression of imprinted tumor suppressor genes, apoptosis, G2/M arrest, and autophagy
by Chen, Min‐Yu and Liao, Warren S.‐L and Lu, Zhen and Bornmann, William G and Hennessey, Violeta and Washington, Michele N and Rosner, Gary L and Yu, Yinhua and Ahmed, Ahmed Ashour and Bast, Robert C
Cancer, ISSN 0008-543X, 10/2011, Volume 117, Issue 19, pp. 4424 - 4438
BACKGROUND: Epigenetic therapy has had a significant impact on the management of hematologic malignancies, but its role in the treatment of ovarian cancer... 
autophagy | PEG3 | ovarian cancer | suberoylanilide hydroxamic acid | decitabine | imprinted tumor suppressor genes | ARHI | DNA METHYLATION | 5-AZA-2'-DEOXYCYTIDINE | ACETYLATION | PHASE-II | COMBINATION | MYELODYSPLASTIC SYNDROME | ONCOLOGY | DEMETHYLATING AGENTS | HISTONE DEACETYLASE INHIBITORS | EPITHELIAL OVARIAN | Genomic Imprinting | Apoptosis - drug effects | Humans | Ovarian Neoplasms - pathology | Decitabine | Transplantation, Heterologous | Autophagy | G2 Phase - drug effects | Genes, Tumor Suppressor - drug effects | Ovarian Neoplasms - genetics | Antimetabolites, Antineoplastic - pharmacology | Female | Gene Expression Regulation, Neoplastic - drug effects | Drug Therapy, Combination | Hydroxamic Acids - pharmacology | Ovarian Neoplasms - drug therapy | Epigenomics | Azacitidine - analogs & derivatives | Cell Division - drug effects | Drug Synergism | Azacitidine - pharmacology | Animals | Mice, Nude | Vorinostat | Cell Line, Tumor | Histone Deacetylase Inhibitors - pharmacology | Cell Proliferation - drug effects | Mice | Mice, Inbred BALB C | decitabine (DAC) | suberoylanilide hydroxamic acid (SAHA)
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5. Full Text Epigenetic reactivation of tumor suppressor genes by a novel small-molecule inhibitor of human DNA methyltransferases
by Brueckner, Bodo and Boy, Regine Garcia and Siedlecki, Pawel and Musch, Tanja and Kliem, H. Christian and Zielenkiewicz, Piotr and Suhai, Sandor and Wiessler, Manfred and Lyko, Frank
Cancer Research, ISSN 0008-5472, 07/2005, Volume 65, Issue 14, pp. 6305 - 6311
DNA methylation regulates gene expression in normal and malignant cells. The possibility to reactivate epigenetically silenced genes has generated considerable... 
METHYLATION | DNMT1 | HYPERMETHYLATION | REPLICATION | THERAPY | ONCOLOGY | SITES | HUMAN CANCER-CELLS | ZEBULARINE | MAMMALIAN-CELLS | SILENCED GENES | Propionates - pharmacology | DNA Modification Methylases - antagonists & inhibitors | Phthalimides | Tryptophan - analogs & derivatives | HCT116 Cells | Humans | Enzyme Inhibitors - pharmacology | Indoles - pharmacology | Gene Expression Regulation, Neoplastic - drug effects | Binding Sites | DNA Methylation - drug effects | Genes, Tumor Suppressor - drug effects
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6. Full Text Tumor Suppressor Gene Inactivation during Cadmium-Induced Malignant Transformation of Human Prostate Cells Correlates with Overexpression of de Novo DNA Methyltransferase
by Lamia Benbrahim-Tallaa and Robert A. Waterland and Anna L. Dill and Mukta M. Webber and Michael P. Waalkes
Environmental Health Perspectives, ISSN 0091-6765, 10/2007, Volume 115, Issue 10, pp. 1454 - 1459
Background: Aberrant DNA methylation is common in carcinogenesis. The typical pattern appears to involve reduced expression of maintenance DNA... 
Cadmium | Epithelial cells | DNA | Tumor suppressor genes | Promoter regions | Research | Methylation | Prostate | Liver cells | Prostate cancer | Cancer | p16 | RASSF1A | DNA methylation | DNMT3b | Carcinogenesis | Up-Regulation | Cadmium - toxicity | DNA (Cytosine-5-)-Methyltransferase 1 | Epithelial Cells - drug effects | Humans | Cells, Cultured | Male | Cell Transformation, Neoplastic - chemically induced | Gene Expression Profiling | Carcinogens, Environmental - toxicity | Case-Control Studies | Genes, Tumor Suppressor - drug effects | DNA (Cytosine-5-)-Methyltransferases - metabolism | Gene Expression Regulation - drug effects | Cell Transformation, Neoplastic - genetics | Prostate - cytology | Prostate - drug effects | DNA (Cytosine-5-)-Methyltransferases - drug effects | DNA Methylation - drug effects | Methyltransferases | Physiological aspects | Chemical properties | Health aspects | carcinogenesis | cadmium | prostate
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7. Full Text (−)-Epigallocatechin-3-gallate reverses the expression of various tumor-suppressor genes by inhibiting DNA methyltransferases and histone deacetylases in human cervical cancer cells
by KHAN, MUNAWWAR ALI and HUSSAIN, ARIF and SUNDARAM, MADHUMITHA KEDHARI and ALALAMI, USAMA and GUNASEKERA, DIAN and RAMESH, LAVEENA and HAMZA, AMINA and QURAISHI, UZMA
Oncology Reports, ISSN 1021-335X, 4/2015, Volume 33, Issue 4, pp. 1976 - 1984
There has been increasing evidence that numerous bioactive dietary agents can hamper the process of carcino-genesis by targeting epigenetic alterations... 
DNMT3B | dietary agents | reactivation | HDAC1 | epigenetic | EGCG | Dietary agents | DNMT3β | Reactivation | Epigenetic | TEA POLYPHENOL | METHYLATION | GREEN TEA | LUNG-CANCER | OVEREXPRESSION | IN-VITRO | RETINOIC ACID | ONCOLOGY | EPIGENETIC REGULATION | HUMAN-MELANOMA | DNA (Cytosine-5-)-Methyltransferases - physiology | Humans | Uterine Cervical Neoplasms - pathology | DNA (Cytosine-5-)-Methyltransferases - antagonists & inhibitors | Chromatin Assembly and Disassembly - drug effects | Genes, Tumor Suppressor - drug effects | RNA, Messenger - biosynthesis | Tumor Suppressor Proteins - genetics | Enzyme Induction - drug effects | Female | Epigenesis, Genetic - drug effects | Gene Expression Regulation, Neoplastic - drug effects | Catechin - pharmacology | Neoplasm Proteins - genetics | Anticarcinogenic Agents - pharmacology | Histone Deacetylase 1 - genetics | DNA (Cytosine-5-)-Methyltransferases - biosynthesis | Neoplasm Proteins - biosynthesis | Models, Molecular | Histone Deacetylase 1 - biosynthesis | Uterine Cervical Neoplasms - genetics | DNA (Cytosine-5-)-Methyltransferases - genetics | RNA, Neoplasm - biosynthesis | Histone Deacetylase Inhibitors - pharmacology | Protein Conformation | Catechin - analogs & derivatives | Molecular Docking Simulation | HeLa Cells | Histone Deacetylases - physiology | Tumor Suppressor Proteins - biosynthesis | DNA Methylation - drug effects | Pharmacology, Experimental | Oncology, Experimental | Development and progression | Tumor suppressor genes | Drug targeting | Genetic aspects | Research | Health aspects | Cervical cancer | Cancer | Studies | Proteins | Enzymes | Cell cycle | DNA methylation | Polyphenols | Epigenetics | Ligands | Gene expression | Kinases | Deoxyribonucleic acid--DNA | Index Medicus
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8. Full Text Nanaomycin A selectively inhibits DNMT3B and reactivates silenced tumor suppressor genes in human cancer cells
by Kuck, Dirk and Caulfield, Thomas and Lyko, Frank and Medina-Franco, Jose L
Molecular Cancer Therapeutics, ISSN 1535-7163, 11/2010, Volume 9, Issue 11, pp. 3015 - 3023
Enzymes involved in the epigenetic regulation of the genome represent promising starting points for therapeutic intervention by small molecules, and DNA... 
INACTIVATION | LUNG | METHYLATION | ANTIBIOTICS | CHROMATIN | ONCOLOGY | PROMOTER DEMETHYLATION | TRANSCRIPTION | MITHRAMYCIN | DNA METHYLTRANSFERASE INHIBITORS | G-C | Gene Silencing - drug effects | HCT116 Cells | Humans | Transcriptional Activation - drug effects | Enzyme Inhibitors - pharmacology | Substrate Specificity | Naphthoquinones - pharmacology | DNA (Cytosine-5-)-Methyltransferases - antagonists & inhibitors | Genes, Tumor Suppressor - drug effects | Neoplasms - genetics | Models, Biological | HL-60 Cells | Inhibitory Concentration 50 | Antineoplastic Agents - pharmacology | Gene Expression Regulation, Neoplastic - drug effects | HeLa Cells | Tumor Cells, Cultured | Drug Evaluation, Preclinical | Neoplasms - pathology | DNA Methylation - drug effects
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9. Full Text Moringa oleifera Gold Nanoparticles Modulate Oncogenes, Tumor Suppressor Genes, and Caspase‐9 Splice Variants in A549 Cells
by Tiloke, Charlette and Phulukdaree, Alisa and Anand, Krishnan and Gengan, Robert M and Chuturgoon, Anil A
Journal of Cellular Biochemistry, ISSN 0730-2312, 10/2016, Volume 117, Issue 10, pp. 2302 - 2314
ABSTRACT Gold nanoparticles (AuNP's) facilitate cancer cell recognition and can be manufactured by green synthesis using nutrient rich medicinal plants such as... 
GOLD NANOPARTICLES | MORINGA OLEIFERA | APOPTOSIS | c‐myc | SPLICE VARIANTS | LUNG CANCER | c-myc | PROTEIN | BIOCHEMISTRY & MOLECULAR BIOLOGY | DNA-DAMAGE | LUNG-CANCER CELLS | SILVER NANOPARTICLES | CELL BIOLOGY | ARREST | IN-VITRO | HELA | MESSENGER-RNA | SRP30A | Leukocytes, Mononuclear - metabolism | Lung Neoplasms - drug therapy | Caspase 9 - genetics | Apoptosis - drug effects | Plant Extracts - pharmacology | Humans | Lung Neoplasms - metabolism | Lung Neoplasms - pathology | Male | Esophageal Neoplasms - pathology | Genes, Tumor Suppressor - drug effects | Moringa oleifera - chemistry | Esophageal Neoplasms - metabolism | RNA Splicing - genetics | Gene Expression Regulation, Neoplastic - drug effects | Tumor Cells, Cultured | Gold - chemistry | Lung Neoplasms - genetics | A549 Cells | Leukocytes, Mononuclear - drug effects | Cytochromes c - metabolism | Metal Nanoparticles - chemistry | Blotting, Western | Metal Nanoparticles - administration & dosage | Esophageal Neoplasms - genetics | Oncogenes - drug effects | Cell Proliferation - drug effects | Antineoplastic Agents, Phytogenic - pharmacology | Esophageal Neoplasms - drug therapy | Nanoparticles | RNA | Genes | Heat shock proteins | Genetic aspects | Genetic engineering | Tumor proteins | Tumors | Proteins | Rodents | Cancer | Apoptosis
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10. Full Text MicroRNA-193a represses c-kit expression and functions as a methylation-silenced tumor suppressor in acute myeloid leukemia
by Gao, X.-N and Lin, J and Li, Y.-H and Gao, L and Wang, X.-R and Wang, W and Kang, H.-Y and Yan, G.-T and Wang, L.-L and Yu, L
Oncogene, ISSN 0950-9232, 08/2011, Volume 30, Issue 31, pp. 3416 - 3428
Aberrant activation of c-kit proto-oncogene contributes to abnormal cell proliferation by altering the tyrosine kinase signaling and constitutes a crucial... 
microRNAs | proto-oncogenes | DNA methylation | tumor suppressor genes | acute myeloid leukemia | c-kit | AML | PROGNOSTIC IMPACT | HYPERMETHYLATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | T(8/21) | CELL-LINES | CELL BIOLOGY | ONCOLOGY | ACUTE LYMPHOBLASTIC-LEUKEMIA | GENETICS & HEREDITY | GENE-EXPRESSION | MUTATIONS | HUMAN CANCER | Gene Silencing - drug effects | Humans | Leukemia, Myeloid, Acute - metabolism | Middle Aged | Male | MicroRNAs - metabolism | Monocytes - metabolism | Proto-Oncogene Proteins c-kit - biosynthesis | Genes, Tumor Suppressor - drug effects | Young Adult | DNA Methylation | Leukemia, Myeloid, Acute - drug therapy | Adult | Bone Marrow Cells - drug effects | Female | Antineoplastic Agents - pharmacology | Promoter Regions, Genetic | Cells, Cultured | Monocytes - drug effects | Azacitidine - pharmacology | Adolescent | Cell Line, Tumor | CpG Islands | Aged | Bone Marrow Cells - metabolism | Research | Gene expression | Methylation | Health aspects | Luciferase | Epigenetics | Oncology | Ribonucleic acid--RNA | Leukemia | Tumors
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11. Full Text A new class of quinoline-based DNA hypomethylating agents reactivates tumor suppressor genes by blocking DNA methyltransferase 1 activity and inducing its degradation
by Datta, Jharna and Ghoshal, Kalpana and Denny, William A and Gamage, Swarna A and Brooke, Darby G and Phiasivongsa, Pasit and Redkar, Sanjeev and Jacob, Samson T
Cancer Research, ISSN 0008-5472, 05/2009, Volume 69, Issue 10, pp. 4277 - 4285
Reactivation of silenced tumor suppressor genes by 5-azacytidine (Vidaza) and its congener 5-aza-2'-deoxycytidine (decitabine) has provided an alternate... 
METHYLATION | THERAPY | 5-AZA-2'-DEOXYCYTIDINE | ONCOLOGY | DEMETHYLATION | CANCER-CELL LINES | IN-VIVO | RAT HEPATOMA | RECEPTOR-TYPE-O | INHIBITORS | HISTONE DEACETYLASE | Gene Silencing - drug effects | DNA Modification Methylases - metabolism | DNA (Cytosine-5-)-Methyltransferase 1 | Humans | DNA (Cytosine-5-)-Methyltransferases - antagonists & inhibitors | Breast Neoplasms | Liver Neoplasms | Reverse Transcriptase Polymerase Chain Reaction | Azacitidine - toxicity | Genes, Tumor Suppressor - drug effects | DNA (Cytosine-5-)-Methyltransferases - genetics | Animals | Cell Line, Tumor | DNA (Cytosine-5-)-Methyltransferases - drug effects | Female | DNA (Cytosine-5-)-Methyltransferases - isolation & purification | Mice | Carcinoma, Hepatocellular | HeLa Cells | Quinolines - toxicity | DNA Methylation - drug effects | Colonic Neoplasms | Index Medicus
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12. Full Text Genistein induces the p21WAF1/CIP1 and p16INK4a tumor suppressor genes in prostate cancer cells by epigenetic mechanisms involving active chromatin modification
by Majid, Shahana and Kikuno, Nobuyuki and Nelles, Jason and Noonan, Emily and Tanaka, Yuichiro and Kawamoto, Ken and Hirata, Hiroshi and Li, Long C and Zhao, Hong and Okino, Steve T and Place, Robert F and Pookot, Deepa and Dahiya, Rajvir
Cancer Research, ISSN 0008-5472, 04/2008, Volume 68, Issue 8, pp. 2736 - 2744
Genistein (4',5,7-trihydroxyisoflavone) is the most abundant isoflavone found in the soybean. The effects of genistein on various cancer cell lines have been... 
APOPTOSIS | GROWTH-FACTOR-BETA | ONCOLOGY | MYELOID-LEUKEMIA | SOY ISOFLAVONES | POTENTIAL MEDIATOR | MELANOMA-CELLS | DEPENDENT KINASE INHIBITOR | PROMOTER | HISTONE ACETYLATION | UP-REGULATION | Prostatic Neoplasms - pathology | Humans | Cyclin-Dependent Kinase Inhibitor p16 - genetics | DNA, Neoplasm - isolation & purification | Male | Gene Expression Profiling | DNA, Neoplasm - drug effects | Genes, Tumor Suppressor - drug effects | Histones - drug effects | Cyclin-Dependent Kinase Inhibitor p21 - genetics | Prostatic Neoplasms - genetics | Genes, Suppressor - drug effects | Genistein - pharmacology | Polymerase Chain Reaction | Cell Line, Tumor | Acetylation | DNA, Neoplasm - genetics | Histones - metabolism | Cell Cycle - drug effects | Chromatin - drug effects | Chromatin - genetics
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13. Full Text Hypoxic silencing of tumor suppressor RUNX3 by histone modification in gastric cancer cells
by Lee, S.H and Kim, J and Kim, W.-H and Lee, Y.M
Oncogene, ISSN 0950-9232, 01/2009, Volume 28, Issue 2, pp. 184 - 194
RUNX3 is a tumor suppressor that is silenced in cancer following hypermethylation of its promoter. The effects of hypoxia in tumor suppressor gene (TSG)... 
Hypoxia |