Long noncoding RNA Linc00460 promotes breast cancer progression by regulating the miR-489-5p/FGF7/AKT axis
文献类型:期刊论文
作者 | Zhu, Yong2; Yang, Leiyan2; Chong, Qing-Yun3,4; Yan, Hong5; Zhang, Weijie2; Qian, Wenchang2; Tan, Sheng2; Wu, Zhengsheng1; Lobie, Peter E.6; Zhu, Tao2 |
刊名 | CANCER MANAGEMENT AND RESEARCH |
出版日期 | 2019 |
卷号 | 11页码:5983-6001 |
ISSN号 | 1179-1322 |
关键词 | Linc00460 miR-489-5p breast cancer FGF7 AKT |
DOI | 10.2147/CMAR.S207084 |
通讯作者 | Lobie, Peter E.(pelobie@sz.tsinghua.edu.cn) ; Zhu, Tao(zhut@ustc.edu.cn) |
英文摘要 | Purpose: Evidence indicates that long noncoding RNAs (lncRNA) possess important roles in various cellular processes and that dysregulation of lncRNAs promotes tumor progression. However, the expression patterns and biological functions of many specific lncRNAs in breast cancer remain to be determined. Methods: Quantitative real-time polymerase chain reaction was performed to detect Linc00460, miR-489-5p and FGF7 expression. Protein levels were determined using Western blot. MTT and colony formation assay were used to measure cell proliferation. Transwell assays were conducted to determine cell migration and invasion. Luciferase reporter assays were carried out to assess the interaction between miR-489-5p and Linc00460 or FGF7. Biotin pull-down assay was used to detect the direct interaction between miR-489-5p and Linc00460. In vivo experiments were performed to measure tumor formation and lung metastasis. Results: We demonstrated that lncRNA Linc00460 was upregulated in breast cancer, and its expression level was positively associated with lymphatic metastasis and poor overall survival. Forced expression of Linc00460 increased, whereas Linc00460 silencing decreased, breast cancer cell viability, migration and invasion both in vitro and in vivo. Linc00460 was identified as a direct target of miR-489-5p, which further targeted FGF7 and exerted oncogenic functions in breast cancer. Mechanistically, Linc00460 served as a competing endogenous RNA of FGF-7 mRNA by sponging miR-489-5p, resulting in upregulated FGF7 expression and AKT activity. Notably, forced expression of miR-489-5p abrogated Linc00460-mediated oncogenic behavior and activation of the FGF7-AKT pathway in breast cancer cells. Conclusion: We have demonstrated that Linc00460 promotes breast cancer progression partly through the miR-489-5p/FGF7/AKT axis. |
WOS关键词 | GROWTH-FACTOR ; GLOBAL PATTERNS ; UP-REGULATION ; EXPRESSION ; INVASION ; RECEPTOR ; PROLIFERATION ; METASTASIS ; ACTIVATION ; MICRORNAS |
资助项目 | National Key Scientific Programme of China[2016YFC1302305] ; National Natural Science Foundation of China[81672615] ; National Natural Science Foundation of China[81472494] ; National Natural Science Foundation of China[81672609] ; Shenzhen Development and Reform Commission Subject Construction Project[[2017]1434] |
WOS研究方向 | Oncology |
语种 | 英语 |
出版者 | DOVE MEDICAL PRESS LTD |
WOS记录号 | WOS:000473725300001 |
资助机构 | National Key Scientific Programme of China ; National Key Scientific Programme of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; Shenzhen Development and Reform Commission Subject Construction Project ; Shenzhen Development and Reform Commission Subject Construction Project ; National Key Scientific Programme of China ; National Key Scientific Programme of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; Shenzhen Development and Reform Commission Subject Construction Project ; Shenzhen Development and Reform Commission Subject Construction Project ; National Key Scientific Programme of China ; National Key Scientific Programme of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; Shenzhen Development and Reform Commission Subject Construction Project ; Shenzhen Development and Reform Commission Subject Construction Project ; National Key Scientific Programme of China ; National Key Scientific Programme of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; Shenzhen Development and Reform Commission Subject Construction Project ; Shenzhen Development and Reform Commission Subject Construction Project |
源URL | [http://cas-ir.dicp.ac.cn/handle/321008/175231] |
专题 | 大连化学物理研究所_中国科学院大连化学物理研究所 |
通讯作者 | Lobie, Peter E.; Zhu, Tao |
作者单位 | 1.Anhui Med Univ, Dept Pathol, Hefei 230032, Anhui, Peoples R China 2.Univ Sci & Technol China, Sch Life Sci, CAS Key Lab Innate Immun & Chron Dis, Hefei Natl Lab Phys Sci Microscale, Hefei 230027, Anhui, Peoples R China 3.Natl Univ Singapore, Canc Sci Inst Singapore, Singapore, Singapore 4.Natl Univ Singapore, Dept Pharmacol, Singapore, Singapore 5.Univ Sci & Technol China, Affiliated Hosp 1, Dept Pathol, Hefei, Anhui, Peoples R China 6.Tsinghua Univ, Tsinghua Berkeley Shenzhen Inst, 1001 Xueyuan Blvd, Shenzhen 518055, Peoples R China |
推荐引用方式 GB/T 7714 | Zhu, Yong,Yang, Leiyan,Chong, Qing-Yun,et al. Long noncoding RNA Linc00460 promotes breast cancer progression by regulating the miR-489-5p/FGF7/AKT axis[J]. CANCER MANAGEMENT AND RESEARCH,2019,11:5983-6001. |
APA | Zhu, Yong.,Yang, Leiyan.,Chong, Qing-Yun.,Yan, Hong.,Zhang, Weijie.,...&Zhu, Tao.(2019).Long noncoding RNA Linc00460 promotes breast cancer progression by regulating the miR-489-5p/FGF7/AKT axis.CANCER MANAGEMENT AND RESEARCH,11,5983-6001. |
MLA | Zhu, Yong,et al."Long noncoding RNA Linc00460 promotes breast cancer progression by regulating the miR-489-5p/FGF7/AKT axis".CANCER MANAGEMENT AND RESEARCH 11(2019):5983-6001. |
入库方式: OAI收割
来源:大连化学物理研究所
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