Abstract
Glioma is the most common and aggressive primary adult brain tumor. Long non-coding RNAs (lncRNAs) have important roles in a variety of biological properties of cancers. Here, we elucidated the function and the possible molecular mechanisms of lncRNA HOTAIR in human glioma U87 and U251 cell lines. Quantitative RT-PCR demonstrated that HOTAIR expression was up-regulated in glioma tissues and cell lines. Knockdown of HOTAIR exerted tumor-suppressive function in glioma cells. Further, HOTAIR was confirmed to be the target of miR-326 and miR-326 mediated the tumor-suppressive effects of HOTAIR knockdown on glioma cell lines. Moreover, over-expressed miR-326 reduced the FGF1 expression which played an oncogenic role in glioma by activating PI3K/AKT and MEK 1/2 pathways. In addition, the in vivo studies also supported the above findings. Taken together, knockdown of HOTAIR up-regulated miR-326 expression, and further inducing the decreased expression of FGF1, these results provided a comprehensive analysis of HOTAIR-miR-326-FGF1 axis in human glioma and provided a new potential therapeutic strategy for glioma treatment.
Highlights
Glioma is the most common and most aggressive malignant primary adult brain tumor
To explore the possible biological significance of HOX transcript antisense intergenic RNA (HOTAIR) in tumorigenesis, we evaluated the effects of HOTAIR inhibition on the cell proliferation, apoptosis, migration, invasion and cell cycle
These results indicated that the knockdown of HOTAIR exerted tumor-suppressive effects in human glioma cells
Summary
Glioma is the most common and most aggressive malignant primary adult brain tumor. The cause of glioma is unknown and the median survival of patients with glioma is less than 15 months under conventional treatments [1, 2]. HOTAIR, a ~2.2-kb long non-coding RNA transcribed from the HOXC locus, is over-expressed in most solid cancers and is correlated with the tumor invasion, progression, metastasis and poor prognosis [8,9,10,11,12]. Recent report has indicated that HOTAIR primarily serves as a prognostic factor for glioma patient survival, a biomarker for identifying glioma molecular subtypes, as well as a critical regulator of cell cycle progression [13]. It could interact with polycomb repressive complex 2 (PRC2) to promote cell cycle progression in glioma [14]. Its biological role in glioma and the underlying molecular mechanism remain undefined
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