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We unexpectedly discovered that normal cellular levels of monomethylated histone H3 lysine 9 (H3K9me1) were also dependent on PR-Set7, but independent of its catalytic activity. This observation suggested that PR-Set7 interacts with an H3K9 monomethyltransferase to establish the previously reported H4K20me1-H3K9me1 trans-tail \u2018histone code\u2019. Here we show that PR-Set7 specifically and directly binds the C-terminus of the Riz1\/PRDM2\/KMT8 tumor suppressor and demonstrate that the N-terminal PR\/SET domain of Riz1 preferentially monomethylates H3K9. The PR-Set7 binding domain was required for Riz1 nuclear localization and maintenance of the H4K20me1-H3K9me1 trans-tail \u2018histone code\u2019. Although Riz1 can function as a repressor, Riz1\/H3K9me1 was dispensable for the repression of genes regulated by PR-Set7\/H4K20me1. Frameshift mutations resulting in a truncated Riz1 incapable of binding PR-Set7 occur frequently in various aggressive cancers. In these cancer cells, expression of wild-type Riz1 restored tumor suppression by decreasing proliferation and increasing apoptosis. These phenotypes were not observed in cells expressing either the Riz1 PR\/SET domain or PR-Set7 binding domain indicating that Riz1 methyltransferase activity and PR-Set7 binding domain are both essential for Riz1 tumor suppressor function.<\/jats:p>","DOI":"10.1093\/nar\/gkt1377","type":"journal-article","created":{"date-parts":[[2014,1,15]],"date-time":"2014-01-15T06:11:33Z","timestamp":1389766293000},"page":"3580-3589","source":"Crossref","is-referenced-by-count":28,"title":["The PR-Set7 binding domain of Riz1 is required for the H4K20me1-H3K9me1 <i>trans<\/i>-tail \u2018histone code\u2019 and Riz1 tumor suppressor function"],"prefix":"10.1093","volume":"42","author":[{"given":"Lauren M.","family":"Congdon","sequence":"first","affiliation":[{"name":"Department of Biochemistry and Molecular Biology, University of Southern California Keck School of Medicine, Harlyne J. 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The objective of the study was to evaluate the level and the methylation status of RIZ1 and analyze its association with clinicopathological features and the histone in the pituitary adenomas. We found that RIZ1-positive cases were 11\/50 and H-Scores 22.75\u2009\u00b1\u200911.83 in invasive pituitary adenomas and 26\/53 and 66.3\u2009\u00b1\u200921.7 in non-invasive pituitary adenomas (\u03c7<jats:sup>2<\/jats:sup>\u2009=\u20098.182, p\u2009=\u20090.004). RIZ1 and C-myc showed the opposite trend in these cases. The methylation levels of RIZ1 were more than 50% in 30.4% (7\/23) CpG sites through MALDI-TOF Mass array. There was significant difference (p\u2009&lt;\u20090.01) in 4 CpG sites between invasive pituitary adenoma group and non-invasive pituitary adenoma group; furthermore, the relieved methylation levels of H3K4\/H3K9 and enhanced methylation levels of H3K27 in the patients\u2019 serum were found. Furthermore, there was statistic difference of H3K4 and H3K27 methylation between invasive pituitary adenoma and non-invasive pituitary adenoma group (p\u2009&lt;\u20090.01). The average progression-free survival in high RIZ1 group was 52.63\u2009\u00b1\u20097.62\u2009months and 26.06\u2009\u00b1\u20094.23\u2009months in low RIZ1 group (p\u2009&lt;\u20090.05). Promoter region methylation of RIZ1 may play an important role in the epigenetic silencing of RIZ1 expression in pituitary adenomas, which may translate into important diagnostic and therapeutic applications. <\/jats:p>","DOI":"10.1177\/1010428317711794","type":"journal-article","created":{"date-parts":[[2017,7,20]],"date-time":"2017-07-20T16:20:06Z","timestamp":1500567606000},"page":"101042831771179","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":19,"title":["RIZ1 and histone methylation status in pituitary adenomas"],"prefix":"10.1177","volume":"39","author":[{"given":"Yake","family":"Xue","sequence":"first","affiliation":[{"name":"Department of Neurosurgery, The First Affiliated Hospital, Zhengzhou University, Zhengzhou, China"}]},{"given":"Ruokun","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Neurosurgery, The First Affiliated Hospital, Zhengzhou University, Zhengzhou, 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Natural Science Foundation of China","doi-asserted-by":"crossref","award":["81171880"],"award-info":[{"award-number":["81171880"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"crossref"}]},{"name":"National Program on Key Basic Research Project","award":["2011CB51001"],"award-info":[{"award-number":["2011CB51001"]}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Obesity"],"published-print":{"date-parts":[[2016,2]]},"abstract":"<jats:sec><jats:title>Objective<\/jats:title><jats:p>The aim of this study was to investigate the shared molecular pathways of obesity and cancer by exploring the role of RIZ1 in obesity and the phospatidylinositol 3\u2010kinase (PI3K)\/V\u2010Akt murine thymoma viral oncogene homolog (PKB) (AKT)\/mechanistic target of rapamycin (mTOR) pathway.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Male wild type (WT) and <jats:italic>Riz1<jats:sup>\u2212\/\u2212<\/jats:sup><\/jats:italic> mice (KO) were fed a standard diet (STD) or a high\u2010fat (HF) diet for up to 8 months. These mice were studied for phenotypic and molecular changes.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p><jats:italic>Riz1<jats:sup>\u2212\/\u2212<\/jats:sup><\/jats:italic> mice gained more weight on a HF diet compared to WT mice, with higher free fatty acid and increased visceral fat. Metabolic cage analysis of <jats:italic>Riz1<jats:sup>\u2212\/\u2212<\/jats:sup><\/jats:italic> mice showed lower oxygen consumption but no changes in food intake and ambulatory activity. <jats:italic>Riz1<jats:sup>\u2212\/\u2212<\/jats:sup><\/jats:italic> mice showed impaired glucose regulation but no change in insulin sensitivity. RNA\u2010seq and quantitative RT\u2010PCR analysis found altered expression in certain glycolysis and ATP production genes such as <jats:italic>Ubiad1<\/jats:italic>, <jats:italic>Atp5g2<\/jats:italic>, and <jats:italic>Cyp4a12<\/jats:italic>. The PI3K\/AKT\/mTOR pathway was activated in the <jats:italic>Riz1<jats:sup>\u2212\/\u2212<\/jats:sup><\/jats:italic> mice fed a HF diet with higher <jats:italic>Akt3<\/jats:italic> mRNA levels and increased phosphorylation of AKT (Ser473), mTOR, and S6.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>The results identify RIZ1 as an important regulator of both <jats:italic>Akt3<\/jats:italic> transcription and AKT phosphorylation and suggest a role for RIZ1 in HF\u2010induced obesity and the AKT pathway.<\/jats:p><\/jats:sec>","DOI":"10.1002\/oby.21364","type":"journal-article","created":{"date-parts":[[2015,12,26]],"date-time":"2015-12-26T13:34:44Z","timestamp":1451136884000},"page":"389-397","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":13,"title":["Tumor suppressor RIZ1 in obesity and the PI3K\/AKT\/mTOR 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Feeding rodents with amino acid defined and methyl-imbalanced diet decreases hepatic SAM and causes liver cancers. RIZ1 (PRDM2 or KMT8) is a tumor suppressor and functions in transcriptional repression by methylating histone H3 lysine 9. Here we show that a methyl-balanced diet conferred additional survival benefits compared to a tumor-inducing methyl-imbalanced diet only in mice with wild type RIZ1 but not in mice deficient in RIZ1. While absence of RIZ1 was tumorigenic in mice fed the balanced diet, its presence did not prevent tumor formation in mice fed the imbalanced diet. Unlike most of its related enzymes, RIZ1 was upregulated by methyl-balanced diet. Methyl-balanced diet did not fully repress oncogenes such as c-Jun in the absence of RIZ1. The data identify RIZ1 as a critical target of methyl-balanced diet in cancer prevention. 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RIZ1: a potential tumor suppressor in glioma. 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Sci."],"published-print":{"date-parts":[[2011]]},"DOI":"10.7150\/ijms.8.161","type":"journal-article","created":{"date-parts":[[2012,1,7]],"date-time":"2012-01-07T05:47:17Z","timestamp":1325915237000},"page":"161-167","source":"Crossref","is-referenced-by-count":12,"title":["Anticancer Activity of the PR Domain of Tumor Suppressor RIZ1"],"prefix":"10.7150","volume":"8","author":[{"given":"Wanpeng","family":"Sun","sequence":"first","affiliation":[]},{"given":"Ling","family":"Qiao","sequence":"additional","affiliation":[]},{"given":"Qiang","family":"Liu","sequence":"additional","affiliation":[]},{"given":"Lifeng","family":"Chen","sequence":"additional","affiliation":[]},{"given":"Binbing","family":"Ling","sequence":"additional","affiliation":[]},{"given":"Ramaswami","family":"Sammynaiken","sequence":"additional","affiliation":[]},{"given":"Jian","family":"Yang","sequence":"additional","affiliation":[]}],"member":"4137","container-title":["International Journal of Medical Sciences"],"language":"en","link":[{"URL":"http:\/\/www.medsci.org\/v08p0161.htm","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2017,3,26]],"date-time":"2017-03-26T20:35:37Z","timestamp":1490560537000},"score":13.658273,"resource":{"primary":{"URL":"http:\/\/www.medsci.org\/v08p0161.htm"}},"issued":{"date-parts":[[2011]]},"references-count":0,"journal-issue":{"issue":"2"},"URL":"https:\/\/doi.org\/10.7150\/ijms.8.161","ISSN":["1449-1907"],"issn-type":[{"value":"1449-1907","type":"print"}],"published":{"date-parts":[[2011]]}},{"indexed":{"date-parts":[[2026,1,19]],"date-time":"2026-01-19T02:30:43Z","timestamp":1768789843789,"version":"3.49.0"},"reference-count":15,"publisher":"Walter de Gruyter GmbH","issue":"1","license":[{"start":{"date-parts":[[2016,1,1]],"date-time":"2016-01-01T00:00:00Z","timestamp":1451606400000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/3.0"}],"content-domain":{"domain":[],"crossmark-restriction":false},"published-print":{"date-parts":[[2016,1,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Retinoblastoma protein-interacting zinc finger gene RIZ encodes two different protein products, RIZ1 and RIZ2. Observations suggest that RIZ1 is a tumor suppressor, while RIZ2 acts as a negative regulator of RIZ1 and may play a positive role in oncogenesis. The imbalance amount of RIZ1 and RIZ2 may be involved in cancer development. In this study we detected the expression levels of RIZ1 and RIZ2 mRNA in human esophageal squamous cell carcinoma (ESCC) tissue specimens, reexpressed RIZ1 in the human ESCC cell line EC109 in which RIZ1 mRNA level was not detected, examined the changes of RIZ1 and RIZ2 mRNA expression, investigated the changes of proliferation, and apoptosis of the cells. We found that RIZ1 mRNA expression is commonly decreased or at undetectable level in human esophageal squamous cancer tissue specimens compared to the normal tissue specimens, while RIZ2 is usually expressed. With the forced expression of RIZ1, RIZ2 mRNA expression did not change, The ESCC cell proliferation was inhibited and apoptosis was induced. This unusual yinyang fashion of RIZ1\/RIZ2 may contribute to the progression of ESCC.<\/jats:p>","DOI":"10.1515\/biol-2016-0019","type":"journal-article","created":{"date-parts":[[2016,8,22]],"date-time":"2016-08-22T14:36:41Z","timestamp":1471876601000},"page":"136-141","source":"Crossref","is-referenced-by-count":5,"title":["The unusual yin-yang fashion of RIZ1\/RIZ2 contributes to the progression of esophageal squamous cell carcinoma"],"prefix":"10.1515","volume":"11","author":[{"given":"Yuantao","family":"Cui","sequence":"first","affiliation":[{"name":"1Department of Cardiothoracic Surgery, Tianjin Medical University General Hospital, Tianjin Medical University, Tianjin 300070, P.R. China"}]},{"given":"Min","family":"Ding","sequence":"additional","affiliation":[{"name":"2Key Laboratory of Hormones and Development (Ministry of Health), Tianjin Key Laboratory of Metabolic Diseases, Tianjin Metabolic Diseases Hospital & Tianjin Institute of Endocrinology, Tianjin Medical University, 300070 Tianjin, P.R. China"}]},{"given":"Shangwen","family":"Dong","sequence":"additional","affiliation":[{"name":"1Department of Cardiothoracic Surgery, Tianjin Medical University General Hospital, Tianjin Medical University, Tianjin 300070, P.R. China"}]},{"given":"Yuanguo","family":"Wang","sequence":"additional","affiliation":[{"name":"1Department of Cardiothoracic Surgery, Tianjin Medical University General Hospital, Tianjin Medical University, Tianjin 300070, P.R. China"}]},{"given":"Peng","family":"Zhang","sequence":"additional","affiliation":[{"name":"1Department of Cardiothoracic Surgery, Tianjin Medical University General Hospital, Tianjin Medical University, Tianjin 300070, P.R. China"}]}],"member":"374","reference":[{"key":"ref51","first-page":"53","article-title":"DNA methylation of the RIZ gene is associated with nuclear accumulation of p in prostate cancer et alDNA methylation of the RIZ gene is associated with nuclear accumulation of p in prostate cancerCancer","volume":"6","author":"Hasegawa","year":"2007","journal-title":"Cancer Sci Sci"},{"key":"ref91","first-page":"272","article-title":"The retinoblastoma interacting zinc finger gene RIZ produces a PR domain - lacking product through an internal promoter The retinoblastoma interacting zinc finger gene RIZ produces a PR domain - lacking product through an internal promoterJ","volume":"10","author":"Liu","year":"1997","journal-title":"Biol Chem Biol Chem"},{"key":"ref201","first-page":"41","article-title":"CxxC domain - containing proteins CpG islands and the chromatin connection CxxC domain - containing proteins CpG islands and the chromatin connectionBiochem","volume":"21","author":"Long","year":"2013","journal-title":"Biochem Soc Trans Soc Trans"},{"key":"ref21","first-page":"1","article-title":"Rearrangements of chromosome band in non - 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risk area DNA methylation and loss of protein expression in esophageal squamous cellcarcinogenesis of high - risk areaJ","volume":"19","author":"Guo","year":"2007","journal-title":"Clin Cancer Res Exp Clin Cancer Res"},{"key":"ref131","first-page":"61","article-title":"Global cancer statistics CA Cancer Global cancer statisticsCA Cancer","volume":"14","author":"Jemal","year":"2011","journal-title":"J Clin J Clin"},{"key":"ref101","first-page":"15","article-title":"The yin - yang of PR - domain family genes in tumorigenesis The yin - yang of PR - domain family genes in tumorigenesisHistol","volume":"11","author":"Jiang","year":"2000","journal-title":"Histol Histopathol Histopathol"},{"key":"ref121","first-page":"349","article-title":"Esophageal cancer Esophageal cancerN","volume":"13","author":"Enzinger","year":"2003","journal-title":"Engl J Med Engl J Med"}],"container-title":["Open Life Sciences"],"link":[{"URL":"https:\/\/www.degruyter.com\/view\/journals\/biol\/11\/1\/article-p136.xml","content-type":"text\/html","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/www.degruyter.com\/downloadpdf\/journals\/biol\/11\/1\/article-p136.xml","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,2,27]],"date-time":"2021-02-27T19:45:05Z","timestamp":1614455105000},"score":13.531183,"resource":{"primary":{"URL":"https:\/\/www.degruyter.com\/document\/doi\/10.1515\/biol-2016-0019\/html"}},"issued":{"date-parts":[[2016,1,1]]},"references-count":15,"journal-issue":{"issue":"1"},"URL":"https:\/\/doi.org\/10.1515\/biol-2016-0019","ISSN":["2391-5412"],"issn-type":[{"value":"2391-5412","type":"electronic"}],"published":{"date-parts":[[2016,1,1]]}}],"items-per-page":20,"query":{"start-index":0,"search-terms":null}}}