Mechanistic and functional extrapolation of SET and MYND domaincontaining protein 2 to pancreatic cancer
作者机构：Department of BiochemistryMicrobiologyand ImmunologyWayne State UniversityDetroitMI 48201United States Department of BiochemistryMicrobiologyand ImmunologyWayne State University School of MedicineDetroitMI 48201United States
出 版 物：《World Journal of Gastroenterology》 (世界胃肠病学杂志（英文版）)
年 卷 期：2022年第28卷第29期
页 面：3753-3766页
核心收录：
学科分类：1002[医学-临床医学] 100214[医学-肿瘤学] 10[医学]
主 题：Pancreatic ductal adenocarcinoma Protein lysine methyltransferase Histone/non-histone methylation Oncogenic signaling pathways Methyltransferase inhibitors
摘 要：Pancreatic ductal adenocarcinoma(PDAC)is one of the most lethal neoplasms worldwide and represents the vast majority of pancreatic cancer *** 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 ***,we review the role of SET and MYND domaincontaining protein 2(SMYD2)in initiating and maintaining PDAC development through methylating multiple tumor suppressors and oncogenic *** 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.
维普期刊数据库