Non-Canonical EZH2 Transcriptionally Activates RelB in Triple Negative Breast Cancer.
Non-Canonical EZH2 Transcriptionally Activates RelB in Triple Negative Breast Cancer.
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DOI：
10.1371/journal.pone.0165005
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发表时间：
2016
期刊：
影响因子：
3.7
通讯作者：
Baldwin AS
中科院分区：
文献类型：
--
作者：
Lawrence CL;Baldwin AS
zeste同源性增强子2（EZH 2）是多梳抑制复合物（PRC 2）的甲基转移酶组分，其通过组蛋白H3在赖氨酸23处的三甲基化（H3 K27 me 3）抑制基因转录。EZH 2活性与肿瘤发生有关，认为其阻断某些肿瘤抑制因子的表达。相对于在癌症中的作用，EZH 2的功能是促进自我更新，并已被证明对乳腺癌中的肿瘤起始细胞（TIC）表型很重要。最近，EZH 2的非经典作用已被确定，其中它促进某些基因的转录激活。在这里，我们发现EZH 2通过甲基转移酶非依赖性机制促进非经典NF-κB亚基RelB的转录激活，以驱动三阴性乳腺癌细胞的自我更新和TIC表型。
Enhancer of zeste homology 2 (EZH2) is the methyltransferase component of the polycomb repressive complex (PRC2) which represses gene transcription via histone H3 trimethylation at lysine 23 (H3K27me3). EZH2 activity has been linked with oncogenesis where it is thought to block expression of certain tumor suppressors. Relative to a role in cancer, EZH2 functions to promote self-renewal and has been shown to be important for the tumor-initiating cell (TIC) phenotype in breast cancer. Recently a non-canonical role for EZH2 has been identified where it promotes transcriptional activation of certain genes. Here we show that EZH2, through a methyltransferase-independent mechanism, promotes the transcriptional activation of the non-canonical NF-κB subunit RelB to drive self-renewal and the TIC phenotype of triple-negative breast cancer cells.
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