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Cited by 194

The DOI matches its Crossref record; 16 of the 16 references it cites were found in a registry or an index.

Phosphorylation of EZH2 by AMPK Suppresses PRC2 Methyltransferase Activity and Oncogenic Function

Open access
Wan, Lixin, Xu, Kexin, Wei, Yongkun, Zhang, Jinfang, Han, Tao, Fry, Christopher, Zhang, Zhao, Wang, Yao Vickie, Huang, Liyu, Yuan, Min, Xia, Weiya, Chang, Wei-Chao, Huang, Wen-Chien, Liu, Chien-Liang, Chang, Yuan-Ching, Liu, Jinsong, Wu, Yun, Jin, Victor X., Dai, Xiangpeng, Guo, Jianfeng, Liu, Jia, Jiang, Shulong, Li, Jin, Asara, John M., Brown, Myles, Hung, Mien-Chie, Wei, Wenyi·2018·Molecular Cell
DOI 10.1016/j.molcel.2017.12.024
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Abstract

SUMMARY Sustained energy starvation leads to activation of AMP-activated protein kinase (AMPK), which coordinates energy status with numerous cellular processes including metabolism, protein synthesis, and autophagy. Here, we report that AMPK phosphorylates the histone methyltransferase EZH2 at T311 to disrupt the interaction between EZH2 and SUZ12, another core component of the polycomb repressive complex 2 (PRC2), leading to attenuated PRC2-dependent methylation of histone H3 at Lys27. As such, PRC2 target genes, many of which are known tumor suppressors, were upregulated upon T311-EZH2 phosphorylation, which suppressed tumor cell growth both in cell culture and mouse xenografts. Pathologically, immunohistochemical analyses uncovered a positive correlation between AMPK activity and pT311-EZH2, and higher pT311-EZH2 correlates with better survival in both ovarian and breast cancer patients. Our finding suggests that AMPK agonists might be promising sensitizers for EZH2 targeting cancer therapies.

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Metadata

Authors
Wan, L., Xu, K., Wei, Y., Zhang, J., Han, T., Fry, C., Zhang, Z., Wang, Y. V., Huang, L., Yuan, M., Xia, W., Chang, W.-C., Huang, W.-C., Liu, C.-L., Chang, Y.-C., Liu, J., Wu, Y., Jin, V. X., Dai, X., Guo, J., Liu, J., Jiang, S., Li, J., Asara, J. M., Brown, M., Hung, M.-C., & Wei, W.
Venue
Molecular Cell
Publisher
Elsevier BV
Published
2018-01
Volume
69
Issue
2
Pages
279-291.e5
ISSN
1097-2765 (ISSN-L)
DOI
10.1016/j.molcel.2017.12.024
OpenAlex
W2782584508
Cited by
194
References
16
FWCI
6.98
Type
journal article
Language
en
Status
Retracted
Open access
bronze

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CoChat. (2026). Citation check: Phosphorylation of EZH2 by AMPK Suppresses PRC2 Methyltransferase Activity and Oncogenic Function. https://app.cochat.ai/papers/10.1016/j.molcel.2017.12.024
The paper
Wan, L., Xu, K., Wei, Y., Zhang, J., Han, T., Fry, C., Zhang, Z., Wang, Y. V., Huang, L., Yuan, M., Xia, W., Chang, W.-C., Huang, W.-C., Liu, C.-L., Chang, Y.-C., Liu, J., Wu, Y., Jin, V. X., Dai, X., . . . Wei, W. (2018). Phosphorylation of EZH2 by AMPK Suppresses PRC2 Methyltransferase Activity and Oncogenic Function. Molecular Cell. https://doi.org/10.1016/j.molcel.2017.12.024

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.