miR-93/miR-106b/miR-375-CIC-CRABP1: a novel regulatory axis in prostate cancer progression

被引:88
作者
Choi, Nahyun [1 ]
Park, Jongmin [1 ]
Lee, Jeon-Soo [1 ]
Yoe, Jeehyun [1 ]
Park, Guk Yeol [1 ]
Kim, Eunjeong [1 ]
Jeon, Hyeongrin [2 ]
Cho, Yong Mee [3 ]
Roh, Tae-Young [1 ,2 ]
Lee, Yoontae [1 ,2 ]
机构
[1] Pohang Univ Sci & Technol, Dept Life Sci, Pohang, Kyungbuk, South Korea
[2] Pohang Univ Sci & Technol, Div Integrat Biosci & Biotechnol, Pohang, Kyungbuk, South Korea
[3] Univ Ulsan, Coll Med, Asan Med Ctr, Dept Pathol, Seoul, South Korea
基金
新加坡国家研究基金会;
关键词
prostate cancer; capicua; ETV5; CRABP1; microRNA; MICRORNA EXPRESSION; RETINOIC ACID; CAPICUA; REPRESSOR; GENES; SCA1; PROFILE; FAMILY;
D O I
10.18632/oncotarget.4372
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Capicua (CIC) has been implicated in pathogenesis of spinocerebellar ataxia type-1 (SCA1) neurodegenerative disease and some types of cancer; however, the role of CIC in prostate cancer remains unknown. Here we show that CIC suppresses prostate cancer progression. CIC expression was markedly decreased in human prostatic carcinoma. CIC overexpression suppressed prostate cancer cell proliferation, invasion, and migration, whereas CIC RNAi exerted opposite effects. We found that knock-down of CIC derepresses expression of ETV5 and CRABP1 in LNCaP and PC-3 cells, respectively, thereby promoting cell proliferation and invasion. We also discovered that miR-93, miR-106b, and miR-375, which are known to be frequently overexpressed in prostate cancer patients, cooperatively down-regulate CIC levels to promote cancer progression. Altogether, we suggest miR-93/miR-106b/miR-375-CIC-CRABP1 as a novel key regulatory axis in prostate cancer progression.
引用
收藏
页码:23533 / 23547
页数:15
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