Long non-coding RNA HOTAIR acts as a competing endogenous RNA to promote glioma progression by sponging miR-126-5p.

LncRNA HOX transcript antisense intergenic RNA (HOTAIR) has been shown to play prominent roles in tumorigenesis. However, its precise molecular mechanism in glioma has not been completely elucidated. In this study, we found that HOTAIR was aberrantly up-regulated in glioma tissues and was negatively correlated with miR-126-5p expression. Next, we determined that HOTAIR promote glioma progression by sponging miR-126-5p. Subsequently, glutaminase (GLS) was confirmed to be a direct target of miR-126-5p using bioinformatics software and a luciferase reporter assay. Moreover, HOTAIR could modulate GLS expression by functioning as a competing endogenous RNA (ceRNA) for miR-126-5p. Taken together, our study clarified that the HOTAIR/miR-126/GLS pathway is involved in glioma progression and may potentially serve as a target for glioma therapy.

Liu L ，Cui S ，Wan T ，Li X ，Tian W ，Zhang R ，Luo L ，Shi Y ... -  《-》

LncRNA HOTAIR acts a competing endogenous RNA to control the expression of notch3 via sponging miR-613 in pancreatic cancer.

Cai H ，Yao J ，An Y ，Chen X ，Chen W ，Wu D ，Luo B ，Yang Y ，Jiang Y ，Sun D ，He X ... -  《-》

Long noncoding RNA NEAT1 promotes progression of glioma as a ceRNA by sponging miR-185-5p to stimulate DNMT1/mTOR signaling.

Long noncoding RNA nuclear paraspeckle assembly transcript 1 (NEAT1) is regarded as an oncogene in multiple cancers. Previous studies have shown that NEAT1 is involved in the proliferation and tumorigenesis of glioma cells, while miR-185-5p functions as a tumor suppressor in glioma. However, the underlying molecular mechanism of NEAT1 in glioma, especially in association with miR-185-5p, has not been studied. In this study, we first demonstrated that NEAT1 expression was upregulated, and miR-185-5p downregulated in glioma tissues and cells. More important, NEAT1 expression was negatively correlated with miR-185-5p expression in glioma tissues. In vitro and in vivo experiments verified that NEAT1 was a competing endogenous RNA for miR-185-5p for promoting DNA methyltransferase 1 (DNMT1) expression and activated mammalian target of rapamycin (mTOR) signaling, thus inhibiting apoptosis, and promoting glioma migration, proliferation, and epithelial-mesenchymal transition process. Furthermore, NEAT1 knockdown suppressed tumor growth and reduced the expression of proliferation antigen Ki-67, DNMT1, and mTOR, but upregulated the expression of miR-185-5p in vivo. Finally, with mTOR inhibitor rapamycin, we confirmed that NEAT1 promoted glioma activity through mTOR signaling both in vitro and in vivo. In conclusion, these results suggest that NEAT1 promotes glioma tumorigenesis via miR-185-5p/DNMT1/mTOR signaling, which may provide a new target for the diagnosis and therapy of glioma.

Yu H ，Xu A ，Wu B ，Wang M ，Chen Z ... -  《-》

Long non-coding RNA HOTAIR promotes cell viability, migration and invasion in thyroid cancer cells by sponging miR-17-5p.

Liu X ，Liu G ，Lu Y ，Shi Y ... -  《-》

Long noncoding RNA HOTAIR promotes medulloblastoma growth, migration and invasion by sponging miR-1/miR-206 and targeting YY1.

Long non-coding RNA (LncRNA) HOX transcript antisense RNA (HOTAIR) and Yin Yang 1 (YY1) are reported to be involved in tumorigenesis. However, the effect and molecular mechanism of HOTAIR on YY1 expression remains poorly understood. The study aimed to investigate the functions and molecular mechanism of LncRNA HOTAIR in medulloblastoma progression. qPCR was performed to detect HOTAIR and YY1 mRNA in tissues and cells, as well as that of miR-1 and miR-206 expression levels. Western blot assay was used to test YY1 and EMT-related biomarkers' protein levels. Cell proliferation was tested with CCK-8 assay and colony formation assay. Migration and invasion abilities were tested with Transwell migration and invasion assays. Tumor growth was tested with an in vivo animal study. Cell apoptosis was tested with an Annexin V-FITC/PI kit. Luciferase assay was used to test the luciferase intensity of YY1 and HOTAIR. RNA pull down assay was used to detect the combination between HOTAIR and miR-1/miR-206. In this study, we found that HOTAIR and YY1 were up-regulated in medulloblastoma tissues and cell lines, and HOTAIR increased YY1 expression. The molecular mechanism demonstrated that HOTAIR negatively regulated miR-1 and miR-206 expression, which can directly target YY1 in medulloblastoma cells. Moreover, HOTAIR increased YY1 expression through binding to miR-1 and miR-206. The functional experiments showed that HOTAIR knockdown suppressed medulloblastoma cell proliferation, tumor growth, migration and invasion, and promoted cell apoptosis via the modulation of the miR-1/miR-206-YY1 axis, as well as epithelial to mesenchymal transition (EMT). These data indicate that HOTAIR promotes medulloblastoma progression via acting as a competing endogenous RNA (ceRNA) to regulate YY1 expression through binding to miR-1 and miR-206.

Zhang J ，Li N ，Fu J ，Zhou W ... -  《-》