子宫内膜癌
癌症研究
蛋白质精氨酸甲基转移酶5
生物
癌症
癌变
细胞生长
基因敲除
甲基转移酶
细胞凋亡
精氨酸
甲基化
生物化学
基因
遗传学
氨基酸
作者
Futaba Inoue,Kenbun Sone,Yusuke Toyohara,Saki Tanimoto,Yu Takahashi,Misako Kusakabe,Asako Kukita,Harunori Honjoh,Akira Nishijima,Ayumi Taguchi,Yukio Miyamoto,Michihiro Tanikawa,Takayuki Iriyama,Mayuyo-mori Uchino,Tetsushi Tsuruga,Osamu Wada‐Hiraike,Katsutoshi Oda,Yutaka Osuga
标识
DOI:10.1016/j.bbrc.2022.02.086
摘要
Histone modification is the key epigenetic mechanism that regulates gene expression. Coactivator-associated arginine methyltransferase 1 (CARM1) is an arginine methyltransferase that catalyzes dimethylation of histone H3 (H3R17) at arginine 17. Lately, it has been suggested that CARM1 is associated with human carcinogenesis, and the CARM1-selective inhibitor, TP-064, has been shown to be a potential therapeutic agent for multiple myeloma. However, the physiological significance of CARM1 in endometrial cancer remains unclear. Therefore, we aimed to explore the role of CARM1 and the effect of TP-064 in endometrial cancer. To this end, we analyzed CARM1 expression in endometrial cancer using quantitative real-time polymerase chain reaction and examined the antitumor mechanism with CARM1 knockdown endometrial cancer cells. Moreover, we evaluated the therapeutic capability of TP-064 in endometrial cancer cells. CARM1 was remarkably overexpressed in 52 endometrial cancer tissues compared to normal endometrial tissues. The growth of CARM1 knockdown endometrial cancer cells was suppressed and CARM1 knockdown induced apoptosis. TP-064 also inhibited endometrial cancer cell growth and declined the number of endometrial cancer cell colonies. These data suggest that CARM1 may be a powerful therapeutic target for endometrial cancer.
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