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miR-218 suppresses gastric cancer cell cycle progression through the CDK6/Cyclin D1/E2F1 axis in a feedback loop

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成果类型:
期刊论文
作者:
Deng, Min;Zeng, Chao;Lu, Xihong;He, Xiusheng;Zhang, Ruixin;...
通讯作者:
Liu, Hao;He, Zhimin
作者机构:
[Liu, Hao; Zhang, Ruixin; Zheng, Guopei; Jia, Xiaoting; Deng, Min; Qiu, Qinwei; He, Zhimin; Liu, H] Guangzhou Med Univ, Canc Hosp, Guangzhou, Guangdong, Peoples R China.
[Liu, Hao; Zhang, Ruixin; Zheng, Guopei; Jia, Xiaoting; Deng, Min; Qiu, Qinwei; He, Zhimin; Liu, H] Guangzhou Med Univ, Canc Res Inst, Guangzhou, Guangdong, Peoples R China.
[Zeng, Chao] Guangdong Med Univ, Dept Pathol, Dongguan, Guangdong, Peoples R China.
[Lu, Xihong] Guangzhou Eighth Peoples Hosp, Guangzhou, Guangdong, Peoples R China.
[He, Xiusheng] Univ South China, Canc Res Inst, Hengyang, Hunan, Peoples R China.
通讯机构:
[Liu, H; He, ZM] G
Guangzhou Med Univ, Canc Hosp, Guangzhou, Guangdong, Peoples R China.
Guangzhou Med Univ, Canc Res Inst, Guangzhou, Guangdong, Peoples R China.
语种:
英文
关键词:
miR-218;E2F1;CDK6;Cyclin D1;Gastric cancer
期刊:
Cancer Letters
ISSN:
0304-3835
年:
2017
卷:
403
页码:
175-185
基金类别:
This work was supported by the National Natural Science Foundation of China (81472625, 81101526 and 81672452), the Science and Technology Planning Project of Guangdong Province (2014A020212741), the Scientific Research Project of Guangzhou Municipal University (1201410235), the “Guangzhou Scholar” Research Project of Guangzhou Municipal University (1201561588), and the Science and Technology Program of Guangzhou (201707010354).
机构署名:
本校为其他机构
院系归属:
医学院
摘要:
Studies in several cancers have suggested that miR-218 has anti-tumor activities, but its function is yet to be elucidated. In this study, we investigated the regulation and function of miR-218 (miR-218-5p) in the cell cycle progression of gastric cancer (GC). We found that miR-218 could suppress proliferation of gastric cancer cells, induce cell cycle arrest at the G1 phase and inhibit tumor growth and metastasis in vivo. We also demonstrated that miR-218 specifically targeted the 3'-UTR regions of CDK6 and cyclin D1 and inhibited the expression of these molecules, which in turn repressed the...

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