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Overexpression of novel lncRNA NLIPMT inhibits metastasis by reducing phosphorylated glycogen synthase kinase 3β in breast cancer
Author(s) -
Jiang Yang,
Lin Lili,
Zhong Shen,
Cai Yangjun,
Zhang Fen,
Wang Xiaobo,
Miao Rongrong,
Zhang Baodan,
Gao Shenmeng,
Hu Xiaoqu
Publication year - 2019
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.27738
Subject(s) - gsk 3 , cancer research , ectopic expression , motility , gsk3b , biology , glycogen synthase , metastasis , breast cancer , cell growth , kinase , phosphorylation , cancer , microbiology and biotechnology , gene , biochemistry , genetics
Long noncoding RNAs (lncRNAs) are considered as regulators of gene expression in cancers. However, cancer profiling has little focused on noncoding genes. Here, we reported that RP11–115N4.1 (here renamed novel lncRNA inhibiting proliferation and metastasis [NLIPMT]) was downregulated in breast cancer tissues. Ectopic expression of NLIPMT inhibited mammary cell proliferation, motility in vitro. Moreover, lnc‐NLIPMT reduced the growth of implanted MDA‐MB‐231 cells in vivo. Mechanistically, glycogen synthase kinase 3β (GSK3β) was identified as an effector protein regulated by lnc‐NLIPMT. Inhibition of GSK3β activity restored NLIPMT‐induced inhibition of proliferation and motility in breast cancer cells. These data reveal that lnc‐NLIPMT functions as a driver of breast cancer progression and might serve as a potential target for antimetastatic therapies.