期刊
GENES & DEVELOPMENT
卷 30, 期 7, 页码 772-785出版社
COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1101/gad.275529.115
关键词
Ras; SMYD2; MAPKAPK3; pancreatic cancer; lung adenocarcinoma; lysine methylation
资金
- National Institutes of Health [RO1 CA172560]
- Lustgarten Foundation
- National Institutes of Health Pathway to Independence [K99/R00, K99CA19781601, K99CA190803]
- Tobacco-Related Disease Research Program
- Dean's Fellowship from Stanford University
- Lucile Packard Foundation for Children's Health at Stanford
- ERS-EU RESPIRE2 Marie Sklodowska-Curie Postdoctoral Research Fellowship [MCF 3776-2013]
- People Programme of the European Union's Seventh Framework Programme under REA grant [600368]
- AbbVie [1097737]
- Bayer Pharma AG
- Boehringer Ingelheim
- Canada Foundation for Innovation
- Eshelman Institute for Innovation
- Janssen
- Novartis Pharma AG
- Ontario Ministry of Economic Development and Innovation
- Pfizer
- Sao Paulo Research Foundation-FAPESP
- Takeda
- Wellcome Trust
- Merck
Pancreatic ductal adenocarcinoma (PDAC) is a lethal form of cancer with few therapeutic options. We found that levels of the lysine methyltransferase SMYD2 (SET and MYND domain 2) are elevated in PDAC and that genetic and pharmacological inhibition of SMYD2 restricts PDAC growth. We further identified the stress response kinase MAPKAPK3 (MK3) as a new physiologic substrate of SMYD2 in PDAC cells. Inhibition of MAPKAPK3 impedes PDAC growth, identifying a potential new kinase target in PDAC. Finally, we show that inhibition of SMYD2 cooperates with standard chemotherapy to treat PDAC cells and tumors. These findings uncover a pivotal role for SMYD2 in promoting pancreatic cancer.
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