The expression of RUNDC3B is associated with promoter methylation in lymphoid malignancies
dc.contributor.author | Burmeister, Dane W. | |
dc.contributor.author | Smith, Emily H. | |
dc.contributor.author | Cristel, Robert T. | |
dc.contributor.author | McKay, Stephanie D. | |
dc.contributor.author | Shi, Huidong | |
dc.contributor.author | Arthur, Gerald L. | |
dc.contributor.author | Davis, Justin Wade | |
dc.contributor.author | Taylor, Kristen H. | |
dc.date.accessioned | 2017-04-14T15:09:56Z | |
dc.date.available | 2018-05-04T20:56:58Z | en |
dc.date.issued | 2017-03 | |
dc.identifier.citation | Burmeister, Dane W.; Smith, Emily H.; Cristel, Robert T.; McKay, Stephanie D.; Shi, Huidong; Arthur, Gerald L.; Davis, Justin Wade; Taylor, Kristen H. (2017). "The expression of RUNDC3B is associated with promoter methylation in lymphoid malignancies." Hematological Oncology 35(1): 25-33. | |
dc.identifier.issn | 0278-0232 | |
dc.identifier.issn | 1099-1069 | |
dc.identifier.uri | https://hdl.handle.net/2027.42/136390 | |
dc.description.abstract | DNA methylation is an epigenetic modification that plays an important role in the regulation of gene expression. The function of RUNDC3B has yet to be determined, although its dysregulated expression has been associated with malignant potential of both breast and lung carcinoma. To elucidate the potential of using DNA methylation in RUNDC3B as a biomarker in lymphoid malignancies, the methylation status of six regions spanning the CpG island in the promoter region of RUNDC3B was determined in cancer cell lines. Lymphoid malignancies were found to have more prominent methylation and did not express RUNDC3B compared with myeloid malignancies and solid tumours, supporting the potential use of DNA methylation in this region as a biomarker for lymphoid malignancies. RUNDC3B contains a RUN domain in its N‐terminal region that mediates interaction with Rap2, an important component of the mitogen‐activated protein kinase (MAPK) cascade, which regulates cellular proliferation and differentiation. The protein sequence of RUNDC3B also contains characteristic binding sites for MAPK intermediates. Therefore, it is possible that RUNDC3B serves as a mediator between Rap2 and the MAPK signalling cascade. Three genes with MAPK‐inducible expression were downregulated in a methylated leukaemia cell line (HSPA5, Jun and Fos). Jun and Fos combine to form the activating protein 1 transcription factor, and loss of this factor is associated with the dysregulation of genes involved in differentiation and proliferation. We hypothesize that the loss of RUNDC3B secondary to aberrant hypermethylation of the early growth response 3 transcription factor binding site results in dysregulated MAPK signalling and carcinogenesis in lymphoid malignancies. © 2015 The Authors. Hematological Oncology published by John Wiley & Sons Ltd | |
dc.publisher | Wiley Periodicals, Inc. | |
dc.publisher | Springer | |
dc.subject.other | RUNDC3B | |
dc.subject.other | DNA methylation | |
dc.subject.other | lymphoma | |
dc.subject.other | leukaemia | |
dc.subject.other | B cell | |
dc.subject.other | gene expression | |
dc.title | The expression of RUNDC3B is associated with promoter methylation in lymphoid malignancies | |
dc.type | Article | en_US |
dc.rights.robots | IndexNoFollow | |
dc.subject.hlbsecondlevel | Oncology and Hematology | |
dc.subject.hlbsecondlevel | Ophthalmology | |
dc.subject.hlbsecondlevel | Public Health | |
dc.subject.hlbsecondlevel | Internal Medicine and Specialties | |
dc.subject.hlbsecondlevel | Otolaryngology | |
dc.subject.hlbsecondlevel | Neurosciences | |
dc.subject.hlbsecondlevel | Obstetrics and Gynecology | |
dc.subject.hlbtoplevel | Health Sciences | |
dc.description.peerreviewed | Peer Reviewed | |
dc.description.bitstreamurl | https://deepblue.lib.umich.edu/bitstream/2027.42/136390/1/hon2238.pdf | |
dc.description.bitstreamurl | https://deepblue.lib.umich.edu/bitstream/2027.42/136390/2/hon2238_am.pdf | |
dc.identifier.doi | 10.1002/hon.2238 | |
dc.identifier.source | Hematological Oncology | |
dc.identifier.citedreference | Robertson KD, Wolffe AP. DNA methylation in health and disease. Nat Rev Genet 2000; 1: 11 – 19. | |
dc.identifier.citedreference | Wang MX, Wang HY, Zhao X, et al. Molecular detection of B‐cell neoplasms by specific DNA methylation biomarkers. Int J Clin Exp Pathol 2010; 3: 265 – 279. | |
dc.identifier.citedreference | Raguz S, De Bella MT, Slade MJ, Higgins CF, Coombes RC, Yague E. Expression of RPIP9 (Rap2 interacting protein 9) is activated in breast carcinoma and correlates with a poor prognosis. Int J Cancer 2005; 117: 934 – 941. | |
dc.identifier.citedreference | Rountree MR, Bachman KE, Herman JG, Baylin SB. DNA methylation, chromatin inheritance, and cancer. Oncogene 2001; 20: 3156 – 3165. | |
dc.identifier.citedreference | Walter SD. Point estimation of the odds ratio in sparse 2 × 2 contingency tables. In Biostatistics. MacNeill IB, Umphrey GJ, Reidel D (eds). Springer: Netherlands, 1987; 71 – 102. | |
dc.identifier.citedreference | Fardel O, Lecureur V, Guillouzo A. The P‐glycoprotein multidrug transporter. Gen Pharmacol 1996; 27: 1283 – 1291. | |
dc.identifier.citedreference | Enokida H, Shiina H, Igawa M, et al. CpG hypermethylation of MDR1 gene contributes to the pathogenesis and progression of human prostate cancer. Cancer Res 2004; 64: 5956 – 5962. | |
dc.identifier.citedreference | Reya T, Duncan AW, Ailles L, et al. A role for Wnt signalling in self‐renewal of haematopoietic stem cells. Nature 2003; 423: 409 – 414. | |
dc.identifier.citedreference | Bilic J, Huang YL, Davidson G, et al. Wnt induces LRP6 signalosomes and promotes dishevelled‐dependent LRP6 phosphorylation. Science 2007; 316: 1619 – 1622. | |
dc.identifier.citedreference | Machida N, Umikawa M, Takei K, et al. Mitogen‐activated protein kinase kinase kinase kinase 4 as a putative effector of Rap2 to activate the c‐Jun N‐terminal kinase. J Biol Chem 2004; 279: 15711 – 15714. | |
dc.identifier.citedreference | ENCODE Project Consortium. An integrated encyclopedia of DNA elements in the human genome. Nature 2012; 489: 57 – 74. | |
dc.identifier.citedreference | Patwardhan S, Gashler A, Siegel MG, et al. EGR3, a novel member of the Egr family of genes encoding immediate‐early transcription factors. Oncogene 1991; 6: 917 – 928. | |
dc.identifier.citedreference | Friedman DR, Weinberg JB, Barry WT, et al. A genomic approach to improve prognosis and predict therapeutic response in chronic lymphocytic leukemia. Clin Cancer Res 2009; 15 ( 22 ): 6947 – 6955. | |
dc.identifier.citedreference | Pei L, Choi JH, Liu J, et al. Genome‐wide DNA methylation analysis reveals novel epigenetic changes in chronic lymphocytic leukemia. Epigenetics 2012; 7 ( 6 ): 567 – 578. | |
dc.identifier.citedreference | Toyota M, Kopecky KJ, Toyota MO, Jair KW, Willman CL, Issa JP. Methylation profiling in acute myeloid leukemia. Blood 2001; 97: 2823 – 2829. | |
dc.identifier.citedreference | Taylor KH, Pena‐Hernandez KE, Davis JW, et al. Large‐scale CpG methylation analysis identifies novel candidate genes and reveals methylation hotspots in acute lymphoblastic leukemia. Cancer Res 2007; 67: 2617 – 2625. | |
dc.identifier.citedreference | Khan NI, Bradstock KF, Bendall LJ. Activation of Wnt/beta‐catenin pathway mediates growth and survival in B‐cell progenitor acute lymphoblastic leukaemia. Br J Haematol 2007; 138: 338 – 348. | |
dc.identifier.citedreference | Vinayagam A, Stelzl U, Foulle R, et al. A directed protein interaction network for investigating intracellular signal transduction. Sci Signal 2011; 4: rs8. | |
dc.identifier.citedreference | Evellin S, Nolte J, Tysack K, et al. Stimulation of phospholipase C‐epsilon by the M3 muscarinic acetylcholine receptor mediated by cyclic AMP and the GTPase Rap2B. J Biol Chem 2002; 277: 16805 – 16813. | |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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