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PRMT5 is required for lymphomagenesis triggered by multiple oncogenic drivers
Yan Li1, Nilesh Chitnis1, Hiroshi Nakagawa2
1Department of Cancer Biology, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania.
Cancer Discovery
|January 14, 2015
Summary
Protein arginine methyltransferase 5 (PRMT5) drives lymphoma by suppressing p53. Inactivating PRMT5 inhibits cancer growth, suggesting PRMT5 as a potential therapeutic target for leukemia and lymphoma.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Genetics
Background:
- Protein arginine methyltransferase 5 (PRMT5) is implicated in lymphomagenesis.
- The oncogenic role and therapeutic potential of PRMT5 in leukemia/lymphoma are not fully established.
Purpose of the Study:
- To investigate the oncogenic function of PRMT5 in leukemia/lymphoma.
- To determine if PRMT5 is a viable therapeutic target.
Main Methods:
- Inactivation of PRMT5 in mouse models with oncogenic drivers.
- Molecular analysis of lymphomas, including p53 methylation.
- Correlation analysis with human tumor specimens.
Main Results:
- PRMT5 inactivation inhibits colony formation driven by multiple oncogenes (cyclin D1, c-MYC, NOTCH1, MLL-AF9).
- PRMT5 overexpression cooperates with cyclin D1 to promote lymphomagenesis.
- PRMT5-mediated p53 methylation suppresses proapoptotic genes, sustaining tumor proliferation and bypassing p53 mutations.
- Human tumors show a correlation between cyclin D1 and p53 methylation.
Conclusions:
- PRMT5 plays a critical role in inhibiting p53-dependent tumor suppression.
- PRMT5 is essential for multiple lymphoma/leukemia oncogenic drivers, supporting its development as a therapeutic target.
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