Cross‐talk between Myc and p53 in B‐cell lymphomas

Chronic Diseases and Translational Medicine - Tập 5 - Trang 139-154 - 2019
Li Yu1,2, Tian-Tian Yu1, Ken H. Young2,3
1Department of Hematology, The Second Affiliated Hospital to Nanchang University, Nanchang, Jiangxi 330006, China
2Hematopathology Division and Pathology Department, Duke University School of Medicine, Durham, NC 27710, USA
3Duke University Medical Center and Cancer Institute, Durham, NC 27710, USA

Tóm tắt

AbstractMyc and p53 proteins are closely associated with many physiological cellular functions, including immune response and lymphocyte survival, and are expressed in the lymphoid organs, which are sites for the development and activation of B‐cell malignancies. Genetic alterations and other mechanisms resulting in constitutive activation, rearrangement, or mutation of MYC and TP53 contribute to the development of lymphomas, progression and therapy resistance by gene dysregulation, activation of downstream anti‐apoptotic pathways, and unfavorable microenvironment interactions. The cross‐talk between the Myc and p53 proteins contributes to the inferior prognosis in many types of B‐cell lymphomas. In this review, we present the physiological roles of Myc and p53 proteins, and recent advances in understanding the pathological roles of Myc, p53, and their cross‐talk in lymphoid neoplasms. In addition, we highlight clinical trials of novel agents that directly or indirectly inhibit Myc and/or p53 protein functions and their signaling pathways. Although, to date, these trials have failed to overcome drug resistance, the new results have highlighted the clinical efficiency of targeting diverse mechanisms of action with the goal of optimizing novel therapeutic opportunities to eradicate lymphoma cells.

Tài liệu tham khảo

10.2174/156652406776894563 10.3390/genes8040115 10.1053/j.seminhematol.2015.01.009 10.1016/j.cell.2012.08.033 10.1038/nrc2072 10.1182/blood-2011-11-366062 10.1038/modpathol.2016.178 10.1038/ni.2418 10.1073/pnas.0437996100 10.1101/cshperspect.a014357 10.1073/pnas.79.24.7837 10.1038/nri3814 10.1038/ni.2428 10.1007/s10495-009-0327-9 10.1089/ars.2010.3644 10.1182/blood-2013-05-498329 10.1097/PAP.0b013e3182169948 10.1111/his.13287 10.1038/nature03845 10.1016/j.celrep.2016.02.039 10.1016/j.ccr.2005.08.005 10.1016/j.celrep.2016.05.015 10.3892/ol.2014.2438 10.1016/j.ccr.2012.09.003 10.1038/nrc2715 10.1002/humu.10190 10.1038/leu.2012.25 10.1182/blood-2007-06-093906 10.1177/1947601911408889 10.1200/JCO.2009.27.8762 10.1182/blood-2013-11-539726 10.1038/nrc2716 10.21037/tcr.2016.11.75 10.1126/scisignal.aai8026 10.1016/j.blre.2017.03.001 10.1073/pnas.2030930100 10.1038/nrc3430 10.1016/j.blre.2016.10.001 10.1038/cdd.2013.14 10.1038/sj.onc.1204101 10.1074/jbc.M605707200 10.1016/0092-8674(93)90500-P 10.1038/onc.2015.457 10.1038/onc.2013.482 10.1016/j.canlet.2018.01.013 10.1038/nrc3318 10.1001/jama.2010.1919 10.1073/pnas.242606799 10.4161/cc.6.13.4436 Wong M.Y., 2011, microRNA‐34 family and treatment of cancers with mutant or wild‐type p53 (Review), Int J Oncol, 38, 1189 10.1016/j.immuni.2010.06.013 10.1111/j.1365-2141.2008.07237.x 10.4161/cc.9.14.12267 10.1038/cdd.2009.56 Song W., 2016, Mechanism of action of EBV, Bcl‐2, p53, c‐Myc and Rb in non‐Hodgkin's lymphoma, Eur Rev Med Pharmacol Sci, 20, 1093 10.1182/blood-2014-02-558833 10.18632/oncotarget.6262 10.1309/AJCPPHMZ6VHF0WQV 10.1038/modpathol.2015.118 10.1182/blood-2016-01-643569 10.1016/j.pathol.2017.09.006 10.3109/10428194.2014.970550 10.1016/j.celrep.2014.03.026 10.1084/jem.20052477 Haupt Y., 1993, bmi‐1 transgene induces lymphomas and collaborates with myc in tumorigenesis, Oncogene, 8, 3161 10.1101/gad.13.20.2678 10.1016/j.gendis.2015.04.001 10.1016/j.cell.2011.08.017 10.1016/j.bbadis.2008.08.009 10.1091/mbc.E06-05-0447 10.1182/blood-2010-10-312231 10.3390/molecules190914723 10.4161/cc.27646 10.1002/jcb.25609 Spender L.C., 2014, Developments in Burkitt's lymphoma: novel cooperations in oncogenic MYC signaling, Cancer Manag Res, 6, 27 10.1128/JVI.75.8.3537-3546.2001 10.1371/journal.ppat.1002573 10.1158/0008-5472.CAN-07-6552 10.1038/sj.onc.1207902 10.1128/MCB.00783-06 10.3324/haematol.2017.172882 10.1158/1078-0432.CCR-12-0055 10.18632/oncotarget.14876 10.7554/eLife.21253 10.1038/leu.2012.119 10.1111/j.1365-2141.2011.08689.x 10.1200/JCO.2014.55.5714 Jonge A.V., 2016, Diffuse large B‐cell lymphoma with MYC gene rearrangements: current perspective on treatment of diffuse large B‐cell lymphoma with MYC gene rearrangements; case series and review of the literature, Eur J Cancer, 55, 140 10.1002/cmdc.200600221 10.1016/S1470-2045(14)71182-9 Tucker D.L., 2015, A critical appraisal of ibrutinib in the treatment of mantle cell lymphoma and chronic lymphocytic leukemia, Ther Clin Risk Manag, 11, 979 10.1016/S1470-2045(14)70335-3 10.1038/nrc.2017.109 10.1126/sciadv.1701383 10.1111/j.1349-7006.2009.01150.x 10.1158/1535-7163.MCT-13-0639 10.3109/10428194.2015.1113280 10.1200/JCO.2011.35.9695 10.1371/journal.pone.0103497 Camicia R., 2013, BAL1/ARTD9 represses the anti‐proliferative and pro‐apoptotic IFNγ‐STAT1‐IRF1‐p53 axis in diffuse large B‐cell lymphoma, J Cell Sci, 126, 1969