Long noncoding RNA Linc00460 promotes breast cancer progression by regulating the miR-489-5p/FGF7/AKT axis

doi:10.2147/CMAR.S207084

	Long noncoding RNA Linc00460 promotes breast cancer progression by regulating the miR-489-5p/FGF7/AKT axis
	Zhu, Yong 2; Yang, Leiyan 2; Chong, Qing-Yun 3,4; Yan, Hong 5; Zhang, Weijie 2; Qian, Wenchang 2; Tan, Sheng 2; Wu, Zhengsheng 1; Lobie, Peter E.6; Zhu, Tao 2
刊名	CANCER MANAGEMENT AND RESEARCH
	2019
卷号	11 页码:5983-6001
关键词	Linc00460 miR-489-5p breast cancer FGF7 AKT
ISSN号	1179-1322
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.
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关键词	GROWTH-FACTOR ; GLOBAL PATTERNS ; UP-REGULATION ; EXPRESSION ; INVASION ; RECEPTOR ; PROLIFERATION ; METASTASIS ; ACTIVATION ; MICRORNAS
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
内容类型	期刊论文
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.