中国科学院机构知识库网格
Chinese Academy of Sciences Institutional Repositories Grid
Mir-1 suppresses tumor cell proliferation in colorectal cancer by inhibition of smad3-mediated tumor glycolysis

文献类型:期刊论文

作者Xu, Wanfu1,2,3; Zhang, Zijing1; Zou, Kejian4; Cheng, Yang1,2,3; Yang, Min1; Chen, Huan1; Wang, Hongli1; Zhao, Junhong1; Chen, Peiyu1; He, Liying1
刊名Cell death & disease
出版日期2017-05-01
卷号8页码:10
ISSN号2041-4889
DOI10.1038/cddis.2017.60
通讯作者Geng, lanlan(genglan_2001@hotmail.com) ; Gong, sitang(gongsitang@hotmail.com)
英文摘要Aberrant expression of microrna (mir)-1 has been observed in many human malignancies. however, the function and underlying mechanism of mir-1 remains elusive. to address the specific role of mir-1 in tumor glycolysis using the gain- or loss-of-function studies. metabolic studies combined with gene expression analysis were performed in vitro and in vivo. we demonstrated aberrant expression of mir-1 in aerobic glycolysis, the warburg effect, in cancer cells. mir-1 suppressed aerobic glycolysis and tumor cell proliferation via inactivation of smad3 and targeting hif-1 alpha, leading to reduce hk2 and mct4 expression, which illustrated a novel pathway to mediate aerobic glycolysis in cancer cells. overexpression of mir-1 mimics significantly decreased tumor glycolysis, including lactate production and glucose uptake, and cell proliferation, and these effects were reversed by ectopic expression of smad3. importantly, endogenous smad3 regulated and interacted with hif-1 alpha, resulting in increasing activity of smad3, and this interaction was dramatically abolished by addition of mir-1. we further demonstrated that smad3 was central to the effects of mir-1 in colorectal cancer cells, establishing a previously unappreciated mechanism by which the mir-1/smad3/hif-1 alpha axis facilitates the warburg effect to promote cancer progression in vitro and in vivo. the results indicate that mir-1 may have an essential role as a tumor suppressor, suggesting its potential role in molecular therapy of patients with advanced colorectal cancer.
WOS关键词CYCLIN-DEPENDENT KINASES ; VASCULAR SMOOTH-MUSCLE ; MESENCHYMAL TRANSITION ; INSULIN-RESISTANCE ; SMAD3 DEFICIENCY ; DOWN-REGULATION ; PHOSPHORYLATION ; LINKER ; CARCINOMA ; HIF-1-ALPHA
WOS研究方向Cell Biology
WOS类目Cell Biology
语种英语
WOS记录号WOS:000402195700007
出版者NATURE PUBLISHING GROUP
URI标识http://www.irgrid.ac.cn/handle/1471x/2373434
专题武汉病毒研究所
通讯作者Geng, Lanlan; Gong, Sitang
作者单位1.Guangzhou Med Univ, Guangzhou Women & Childrens Med Ctr, Dept Gastroenterol, Guangzhou 510623, Guangdong, Peoples R China
2.Guangzhou Med Univ, Guangzhou Women & Childrens Med Ctr, Guangzhou Inst Paediat, Guangzhou 510623, Guangdong, Peoples R China
3.Chinese Acad Sci, Wuhan Inst Virol, Wuhan 510623, Guangdong, Peoples R China
4.Hainan Gen Hosp, Dept Gen Surg, Haikou, Hainan, Peoples R China
推荐引用方式
GB/T 7714
Xu, Wanfu,Zhang, Zijing,Zou, Kejian,et al. Mir-1 suppresses tumor cell proliferation in colorectal cancer by inhibition of smad3-mediated tumor glycolysis[J]. Cell death & disease,2017,8:10.
APA Xu, Wanfu.,Zhang, Zijing.,Zou, Kejian.,Cheng, Yang.,Yang, Min.,...&Gong, Sitang.(2017).Mir-1 suppresses tumor cell proliferation in colorectal cancer by inhibition of smad3-mediated tumor glycolysis.Cell death & disease,8,10.
MLA Xu, Wanfu,et al."Mir-1 suppresses tumor cell proliferation in colorectal cancer by inhibition of smad3-mediated tumor glycolysis".Cell death & disease 8(2017):10.

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来源:武汉病毒研究所

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