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首页> 外文期刊>Journal of cellular physiology. >Long noncoding RNA NEAT1 promotes progression of glioma as a ceRNA by sponging miR-185-5p to stimulate DNMT1/ mTOR signaling
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Long noncoding RNA NEAT1 promotes progression of glioma as a ceRNA by sponging miR-185-5p to stimulate DNMT1/ mTOR signaling

机译：长非编码RNA NEAT1促进发展神经胶质瘤的电抗器,骗取mir - 185 - 5 - p刺激DNMT1 / mTOR信号

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摘要

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 upregu-lated, 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/DNMTl/mTOR signaling, which may provide a new target for the diagnosis and therapy of glioma.
机译：长非编码RNA核paraspeckle组装记录1 (NEAT1)被认为是一种癌基因在多种癌症。NEAT1参与核扩散和神经胶质瘤细胞的肿瘤发生,而mir - 185 - 5 - p在神经胶质瘤肿瘤抑制功能。然而,潜在的分子机制NEAT1在神经胶质瘤,尤其是在联系mir - 185 - 5 - p,尚未被研究过。我们首先证明NEAT1表达式upregu-lated, mir - 185 - 5 - p表达下调神经胶质瘤组织和细胞。表达式是负相关mir - 185 - 5 - p神经胶质瘤组织中的表达。和体内实验证实NEAT1是一个内源性RNA竞争mir - 185 - 5 - p促进DNA甲基转移酶1 (DNMT1)哺乳动物的目标表达和激活雷帕霉素(mTOR)信号,从而抑制神经胶质瘤细胞凋亡,促进迁移,扩散,epithelial-mesenchymal过渡的过程。抑制肿瘤的生长,减少了DNMT1增殖抗原的表达ki - 67,和mTOR,但调节的表达mir - 185 - 5 - p体内。雷帕霉素,我们证实NEAT1晋升通过mTOR信号在神经胶质瘤的活动体外和体内。表明NEAT1促进神经胶质瘤肿瘤发生通过mir - 185 - 5 - p / DNMTl / mTOR信号,这可能提供一种新的诊断和目标神经胶质瘤的治疗。

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