TY - JOUR
T1 - Aberrant chromatin remodeling in gynecological cancer (Review)
AU - Okawa, Ryuichiro
AU - Banno, Kouji
AU - Iida, Miho
AU - Yanokura, Megumi
AU - Takeda, Takashi
AU - Iijima, Moito
AU - Irie, Haruko Kunitomi
AU - Nakamura, Kanako
AU - Adachi, Masataka
AU - Umene, Kiyoko
AU - Nogami, Yuya
AU - Masuda, Kenta
AU - Kobayashi, Yusuke
AU - Tominaga, Eiichirou
AU - Aoki, Daisuke
N1 - Funding Information:
The authors would like to thank Dr S. Fujiwara and Dr K. Hoshi (Keio University School of Medicine, Tokyo, Japan) for their assistance, and are grateful for support from the Keio Gijuku Academic Development Fund.
Publisher Copyright:
© 2017, Spandidos Publications. All rights reserved.
PY - 2017/11
Y1 - 2017/11
N2 - 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.
AB - 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.
KW - AT-rich interaction domain 1A
KW - Carcinogenesis
KW - Chromatin remodeling
KW - Gynecological cancer
KW - Mutation
KW - Switch/sucrose non-fermentable complex
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U2 - 10.3892/ol.2017.6891
DO - 10.3892/ol.2017.6891
M3 - Review article
AN - SCOPUS:85030175423
SN - 1792-1074
VL - 14
SP - 5107
EP - 5113
JO - Oncology Letters
JF - Oncology Letters
IS - 5
ER -
