Long non-coding RNA LINK-A promotes glioma cell growth and invasion via lactate dehydrogenase A

被引:18
作者
Wu, Dejun [1 ]
Zhao, Bing [1 ]
Cao, Xiaoyu [3 ]
Wan, Jinghai [1 ,2 ]
机构
[1] Anhui Med Univ, Dept Neurosurg, Affiliated Hosp 2, 678 Furong Rd, Hefei 230601, Anhui, Peoples R China
[2] Chinese Acad Med Sci, Canc Inst & Hosp, Dept Neurosurg, Beijing 100021, Peoples R China
[3] Capital Med Univ, Beijing Tiantan Hosp, Dept Neurosurg, Beijing 100050, Peoples R China
基金
中国国家自然科学基金;
关键词
glioma; lncRNAs; LINK-A; LDH-A; PANCREATIC-CANCER; GLIOBLASTOMA; PROGRESSION; HOTAIR; INACTIVATION; INHIBITION; GLYCOLYSIS;
D O I
10.3892/or.2017.5806
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Long non-coding RNAs (lncRNAs) have recently been identified in mammals as new modulators of cancer origin and progression participating in various cellular pro-cesses. Long intergenic non-coding RNA for kinase activation (LINK-A), belonging to one of the intergenic lncRNAs, was reported to regulate signaling pathways correlated with triple-negative breast cancer. However, the expression and the functional role of LINK-A in glioma are still unclear. In the present study, we demonstrated that LINK-A was upregulated in human glioma cells compared with the expression noted in normal astrocytes. Knockdown of LINK-A inhibited cell proliferation, migration and invasion in U87 and U251 glioma cells. In addition, we found that lactate dehydrogenase A (LDH-A) was regulated by LINK-A, and enforced expression of LDH-A promoted glycolysis and proliferation in glioma cells. More importantly, we found that LDH-A was involved in the LINK-A-mediated proliferation and invasion of glioma cells. Collectively, these results provide new evidence of an important role for LINK-A in the development of glioma.
引用
收藏
页码:1525 / 1532
页数:8
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