| Literature DB >> 29113150 |
Ryuichiro Okawa1, Kouji Banno1, Miho Iida1, Megumi Yanokura1, Takashi Takeda1, Moito Iijima1, Haruko Kunitomi-Irie1, Kanako Nakamura1, Masataka Adachi1, Kiyoko Umene1, Yuya Nogami1, Kenta Masuda1, Yusuke Kobayashi1, Eiichiro Tominaga1, Daisuke Aoki1.
Abstract
Epigenetic regulatory mechanisms are a current focus in studies investigating cancer. Chromatin remodeling alters chromatin structure and regulates gene expression, and aberrant chromatin remodeling is involved in carcinogenesis. AT-rich interactive domain-containing protein 1A (ARID1A) and SWItch/sucrose non-fermentable-related, matrix-associated, actin-dependent regulator of chromatin, subfamily a, member 4 are remodeling factors that are mutated in numerous types of cancer. In gynecological cancer, ARID1A mutations have been identified in 46-57% of clear cell carcinoma and 30% of endometrioid carcinoma. Mutations of chromodomain helicase, DNA-binding protein 4 have been detected in 17-21% of endometrial serous cancer, and mutations of ARID1A and mixed-lineage leukemia 3 occur in 36 and 27% of uterine carcinosarcoma, respectively. These data suggest that aberrant chromatin remodeling is a potential cause of cancer, and have led to the development of novel proteins targeting these processes. Additional accumulation of information on the mechanisms of chromatin remodeling and markers for these events may promote personalized anticancer therapies.Entities:
Keywords: AT-rich interaction domain 1A; carcinogenesis; chromatin remodeling; gynecological cancer; mutation; switch/sucrose non-fermentable complex
Year: 2017 PMID: 29113150 PMCID: PMC5656032 DOI: 10.3892/ol.2017.6891
Source DB: PubMed Journal: Oncol Lett ISSN: 1792-1074 Impact factor: 2.967