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1
JAK3-mediated phosphorylation of EZH2: a novel mechanism of non-canonical EZH2 activation and oncogenic function.JAK3介导的EZH2磷酸化：非经典EZH2激活和致癌功能的新机制。
Transl Cancer Res. 2016 Nov;5(Suppl 6):S1208-S1211. doi: 10.21037/tcr.2016.11.11.
2
Protein kinase A-mediated phosphorylation regulates STAT3 activation and oncogenic EZH2 activity.蛋白激酶 A 介导的磷酸化调节 STAT3 的激活和致癌 EZH2 的活性。
Oncogene. 2018 Jun;37(26):3589-3600. doi: 10.1038/s41388-018-0218-z. Epub 2018 Mar 26.
3
Inhibition of EZH2 via activation of SAPK/JNK and reduction of p65 and DNMT1 as a novel mechanism in inhibition of human lung cancer cells by polyphyllin I.通过激活SAPK/JNK以及降低p65和DNMT1来抑制EZH2，作为重楼皂苷I抑制人肺癌细胞的一种新机制。
J Exp Clin Cancer Res. 2016 Jul 16;35(1):112. doi: 10.1186/s13046-016-0388-x.
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Non-Canonical EZH2 Transcriptionally Activates RelB in Triple Negative Breast Cancer.非经典EZH2在三阴性乳腺癌中对RelB进行转录激活。
PLoS One. 2016 Oct 20;11(10):e0165005. doi: 10.1371/journal.pone.0165005. eCollection 2016.
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Janus kinases in interleukin-2-mediated signaling: JAK1 and JAK3 are differentially regulated by tyrosine phosphorylation.白细胞介素-2介导信号传导中的Janus激酶：JAK1和JAK3受酪氨酸磷酸化的差异调节。
Curr Biol. 1997 Nov 1;7(11):817-26. doi: 10.1016/s0960-9822(06)00369-1.
6
DNA-PK-mediated phosphorylation of EZH2 regulates the DNA damage-induced apoptosis to maintain T-cell genomic integrity.DNA依赖蛋白激酶介导的EZH2磷酸化调节DNA损伤诱导的凋亡以维持T细胞基因组完整性。
Cell Death Dis. 2016 Jul 28;7(7):e2316. doi: 10.1038/cddis.2016.198.
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EZH2 upregulates the PI3K/AKT pathway through IGF1R and MYC in clinically aggressive chronic lymphocytic leukaemia.EZH2 通过 IGF1R 和 MYC 上调临床侵袭性慢性淋巴细胞白血病中的 PI3K/AKT 通路。
Epigenetics. 2019 Nov;14(11):1125-1140. doi: 10.1080/15592294.2019.1633867. Epub 2019 Jun 26.
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Hyperactivation of Oncogenic JAK3 Mutants Depend on ATP Binding to the Pseudokinase Domain.致癌性JAK3突变体的过度激活依赖于ATP与假激酶结构域的结合。
Front Oncol. 2018 Dec 3;8:560. doi: 10.3389/fonc.2018.00560. eCollection 2018.
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EZH2 Phosphorylation Promotes Self-Renewal of Glioma Stem-Like Cells Through NF-κB Methylation.EZH2磷酸化通过NF-κB甲基化促进胶质瘤干细胞样细胞的自我更新。
Front Oncol. 2019 Jul 16;9:641. doi: 10.3389/fonc.2019.00641. eCollection 2019.
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GSK3β inactivation promotes the oncogenic functions of EZH2 and enhances methylation of H3K27 in human breast cancers.糖原合成酶激酶3β失活促进EZH2的致癌功能，并增强人乳腺癌中H3K27的甲基化。
Oncotarget. 2016 Aug 30;7(35):57131-57144. doi: 10.18632/oncotarget.11008.

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1
Antihistamine Drug Ebastine Inhibits Cancer Growth by Targeting Polycomb Group Protein EZH2.抗组胺药物依巴斯汀通过靶向多梳蛋白组蛋白 EZH2 抑制癌症生长。
Mol Cancer Ther. 2020 Oct;19(10):2023-2033. doi: 10.1158/1535-7163.MCT-20-0250. Epub 2020 Aug 27.
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Inhibition of EZH2 induces NK cell-mediated differentiation and death in muscle-invasive bladder cancer.抑制 EZH2 可诱导肌肉浸润性膀胱癌中 NK 细胞介导的分化和死亡。
Cell Death Differ. 2019 Oct;26(10):2100-2114. doi: 10.1038/s41418-019-0278-9. Epub 2019 Jan 28.
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JAK2 regulates mismatch repair protein-mediated epigenetic alterations in response to oxidative damage.JAK2调节错配修复蛋白介导的表观遗传改变以应对氧化损伤。
Environ Mol Mutagen. 2019 May;60(4):308-319. doi: 10.1002/em.22269. Epub 2019 Jan 7.

本文引用的文献

1
Aberrant differential expression of EZH1 and EZH2 in Polycomb repressive complex 2 among B- and T/NK-cell neoplasms.B细胞及T/NK细胞肿瘤中多梳抑制复合体2内EZH1和EZH2的异常差异表达
Pathology. 2016 Aug;48(5):467-82. doi: 10.1016/j.pathol.2016.05.002. Epub 2016 Jun 14.
2
EZH2 phosphorylation by JAK3 mediates a switch to noncanonical function in natural killer/T-cell lymphoma.JAK3 通过磷酸化 EZH2 介导自然杀伤/T 细胞淋巴瘤向非典型功能的转变。
Blood. 2016 Aug 18;128(7):948-58. doi: 10.1182/blood-2016-01-690701. Epub 2016 Jun 13.
3
Modulation of EZH2 Expression by MEK-ERK or PI3K-AKT Signaling in Lung Cancer Is Dictated by Different KRAS Oncogene Mutations.肺癌中MEK-ERK或PI3K-AKT信号对EZH2表达的调节取决于不同的KRAS癌基因突变。
Cancer Res. 2016 Feb 1;76(3):675-85. doi: 10.1158/0008-5472.CAN-15-1141. Epub 2015 Dec 16.
4
Reduced H3K27me3 and DNA hypomethylation are major drivers of gene expression in K27M mutant pediatric high-grade gliomas.K27M 突变型小儿高级别胶质瘤中 H3K27me3 减少和 DNA 低甲基化是基因表达的主要驱动因素。
Cancer Cell. 2013 Nov 11;24(5):660-72. doi: 10.1016/j.ccr.2013.10.006. Epub 2013 Oct 31.
5
In aggressive variants of non-Hodgkin lymphomas, Ezh2 is strongly expressed and polycomb repressive complex PRC1.4 dominates over PRC1.2.在侵袭性非霍奇金淋巴瘤中，Ezh2 强烈表达，多梳抑制复合物 PRC1.4 占主导地位，而 PRC1.2 则处于次要地位。
Virchows Arch. 2013 Nov;463(5):697-711. doi: 10.1007/s00428-013-1428-y. Epub 2013 Aug 16.
6
JAK3 deregulation by activating mutations confers invasive growth advantage in extranodal nasal-type natural killer cell lymphoma.激活突变导致 JAK3 失调，赋予结外鼻型自然杀伤细胞淋巴瘤侵袭性生长优势。
Leukemia. 2014 Feb;28(2):338-48. doi: 10.1038/leu.2013.157. Epub 2013 May 21.
7
Phosphorylation of EZH2 activates STAT3 signaling via STAT3 methylation and promotes tumorigenicity of glioblastoma stem-like cells.EZH2 的磷酸化通过 STAT3 甲基化激活 STAT3 信号通路，并促进神经胶质瘤干细胞样细胞的致瘤性。
Cancer Cell. 2013 Jun 10;23(6):839-52. doi: 10.1016/j.ccr.2013.04.008. Epub 2013 May 16.
8
Inhibition of PRC2 activity by a gain-of-function H3 mutation found in pediatric glioblastoma.功能获得性 H3 突变抑制 PRC2 活性，该突变存在于小儿脑胶质瘤中。
Science. 2013 May 17;340(6134):857-61. doi: 10.1126/science.1232245. Epub 2013 Mar 28.
9
EZH2 overexpression in natural killer/T-cell lymphoma confers growth advantage independently of histone methyltransferase activity.EZH2 在自然杀伤/T 细胞淋巴瘤中的过表达赋予其独立于组蛋白甲基转移酶活性的生长优势。
Blood. 2013 May 30;121(22):4512-20. doi: 10.1182/blood-2012-08-450494. Epub 2013 Mar 25.
10
EZH2 oncogenic activity in castration-resistant prostate cancer cells is Polycomb-independent.在去势抵抗性前列腺癌细胞中，EZH2 致癌活性是独立于 Polycomb 的。
Science. 2012 Dec 14;338(6113):1465-9. doi: 10.1126/science.1227604.

JAK3-mediated phosphorylation of EZH2: a novel mechanism of non-canonical EZH2 activation and oncogenic function.

作者信息

Karantanos Theodoros, Boussiotis Vassiliki A

机构信息

Division of Hematology-Oncology, Harvard Medical School, Boston, MA 02215, USA.

Department of Medicine Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA.

出版信息

Transl Cancer Res. 2016 Nov;5(Suppl 6):S1208-S1211. doi: 10.21037/tcr.2016.11.11.

DOI:10.21037/tcr.2016.11.11
PMID:28868240
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5578425/
Abstract
摘要