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Biomed Pharmacother. 2019 Jun 7;117:109069. doi: 10.1016/j.biopha.2019.109069. [Epub ahead of print]

LncRNA LINC00689 promotes the growth, metastasis and glycolysis of glioma cells by targeting miR-338-3p/PKM2 axis.

Author information

1
Key Laboratory of Tumor Molecular Diagnosis and Individualized Medicine of Zhejiang Province, Zhejiang Provincial People's Hospital (People's Hospital of Hangzhou Medical College), Hangzhou, Zhejiang Province, 310014, China.
2
Department of Second Clinical Medical College, Zhejiang Chinese Medical University, Hangzhou, Zhejiang Province, 310000, China.
3
Graduate Department, BengBu Medical College, BengBu, Anhui Province, 233030, China.
4
The Medical College of Qindao University, Qindao, Shandong Province, 266071, China.
5
Key Laboratory of Tumor Molecular Diagnosis and Individualized Medicine of Zhejiang Province, Zhejiang Provincial People's Hospital (People's Hospital of Hangzhou Medical College), Hangzhou, Zhejiang Province, 310014, China. Electronic address: windway626@sina.com.

Abstract

Accumulating evidence supports that long non-coding RNAs (lncRNAs) are implicated in the tumorigenesis and progression of glioma. Recent studies find that lncRNA long intergenic non-protein coding RNA 689 (LINC00689) is associated with obesity and participates in eukaryotic gene expression. However, whether LINC00689 plays a critical role in glioma progression remains unknown. Here, we identified a highly expressed lncRNA LINC00689 in gliomas compared to normal brain tissues based on the GSE dataset (GSE4290). The analysis of our data indicated that the expression of LINC00689 was up-regulated in glioma tissues and cell lines. Moreover, the high expression of LINC00689 was closely correlated with tumor size ≥3 cm, high tumor grade, low KPS scores and poor prognosis of glioma patients. Further investigation demonstrated that LINC00689 knockdown markedly repressed the proliferation, migration, invasion and glycolysis of glioma cells. Additionally, silencing of LINC00689 significantly suppressed the growth of glioma cells in vivo. Mechanistically, LINC00689 functioned as a competing endogenous RNA (ceRNA) by directly interacting with miR-338-3p to promote pyruvate kinase M2 (PKM2) expression. Notably, we also revealed that restoration of PKM2 abolished the effects of LINC00689 silencing on glioma cell proliferation, migration, invasion and glycolysis. In summary, our results suggested that LINC00689/miR-338-3p/PKM2 axis might play an essential role in glioma progression.

KEYWORDS:

Glioma growth; Glycolysis; LINC00689; Metastasis; PKM2; miR-338-3p

PMID:
31181442
DOI:
10.1016/j.biopha.2019.109069
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