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Abstract
Protein arginine methyl transferase 1 (PRMT1) was shown to be up-regulated in cancers and important for cancer cell proliferation. However, the role of PRMT1 in lung cancer progression and metastasis remains incompletely understood. In the present study, we show that PRMT1 is an important regulator of epithelial-mesenchymal transition (EMT), cancer cell migration, and invasion, which are essential processes during cancer progression, and metastasis. Additionally, we have identified Twist1, a basic helix-loop-helix transcription factor and a well-known E-cadherin repressor, as a novel PRMT1 substrate. Taken together, we show that PRMT1 is a novel regulator of EMT and arginine 34 (Arg-34) methylation of Twist1 as a unique "methyl arginine mark" for active E-cadherin repression. Therefore, targeting PRMT1-mediated Twist1 methylation might represent a novel strategy for developing new anti-invasive/anti-metastatic drugs. Moreover, methylated Twist1 (Arg-34), as such, could also emerge as a potential important biomarker for lung cancer.
Highlights
We show that Protein arginine methyl transferase 1 (PRMT1) is a novel regulator of epithelial-mesenchymal transition (EMT) and arginine 34 (Arg-34) methylation of Twist1 as a unique “methyl arginine mark” for active E-cadherin repression
EMT is increasingly recognized as an essential event in cancer progression and metastasis, we evaluated first the role of PRMT1 on EMT
We identify a novel role for PRMT1 in the regulation of EMT, mechanistically via the Arg-34 methylation of the E-cadherin repressor, Twist1
Summary
Protein arginine methyl transferase 1 (PRMT1) was shown to be up-regulated in cancers and important for cancer cell proliferation. We show that PRMT1 is an important regulator of epithelial-mesenchymal transition (EMT), cancer cell migration, and invasion, which are essential processes during cancer progression, and metastasis. We show that PRMT1 is a novel regulator of EMT and arginine 34 (Arg-34) methylation of Twist as a unique “methyl arginine mark” for active E-cadherin repression. We identified PRMT1 as a novel regulator of Epithelial-Mesenchymal-Transition (EMT), an essential process during cancer progression, and metastasis. PRMT1 is shown to be a novel regulator of EMT and PRMT1 methylation of Twist at arginine 34 (Arg34) as a unique “methyl arginine mark” for active E-cadherin repression
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