Open AccessAberrant chromatin remodeling in gynecological cancer (Review)
Author(s) -
Ryuichiro Okawa,
Kouji Banno,
Miho Iida,
Megumi Yanokura,
Takashi Takeda,
Moito Iijima,
Haruko Kunitomi-Irie,
Kenzo Nakamura,
Manabu Adachi,
Kiyoko Umene,
Yuya Nogami,
Kenta Masuda,
Yusuke Kobayashi,
Eiichiro Tominaga,
Daisuke Aoki
Publication year - 2017
Publication title -
oncology letters
Language(s) - Uncategorized
Resource type - Journals
SCImago Journal Rank - 0.766
H-Index - 54
eISSN - 1792-1082
pISSN - 1792-1074
DOI - 10.3892/ol.2017.6891
Subject(s) - chromodomain , chromatin remodeling , arid1a , chromatin , biology , cancer research , epigenetics , carcinogenesis , cancer , microbiology and biotechnology , genetics , mutation , gene , helicase , rna
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.