Mechanistic and functional extrapolation of SET and MYND domain-containing protein 2 to pancreatic cancer

Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal neoplasms worldwide and represents the vast majority of pancreatic cancer cases. Understanding the molecular pathogenesis and the underlying mechanisms involved in the initiation, maintenance, and progression of PDAC is an urgent need, which may lead to the development of novel therapeutic strategies against this deadly cancer. Here, we review the role of SET and MYND domain-containing protein 2 (SMYD2) in initiating and maintaining PDAC development through methylating multiple tumor suppressors and oncogenic proteins. Given the broad substrate specificity of SMYD2 and its involvement in diverse oncogenic signaling pathways in many other cancers, the mechanistic extrapolation of SMYD2 from these cancers to PDAC may allow for developing new hypotheses about the mechanisms driving PDAC tumor growth and metastasis, supporting a proposition that targeting SMYD2 could be a powerful strategy for the prevention and treatment of PDAC.

Automated summary

This article reviews the role of SMYD2 in initiating and sustaining PDAC development through methylation of multiple tumor suppressors and oncogenic proteins. The mechanistic extrapolation of SMYD2 from other cancers may provide insights into the mechanisms driving PDAC tumor growth and metastasis, suggesting that targeting SMYD2 could be a powerful strategy for preventing and treating PDAC.