长非编码 RNA LINC00473 通过损害 miR-637/CDK6 轴促进神经胶质瘤细胞的增殖和侵袭。
Long non-coding RNA LINC00473 promotes glioma cells proliferation and invasion by impairing miR-637/CDK6 axis.
机构信息
Department of Neurosurgery, The First Affiliated Hospital, College of Clinical Medicine of Henan University of Science and Technology , Luoyang , China.
Department of Neurosurgery, The Second Affiliated Hospital of Zhengzhou University , Zhengzhou , China.
出版信息
Artif Cells Nanomed Biotechnol. 2019 Dec;47(1):3896-3903. doi: 10.1080/21691401.2019.1671431.
LINC00473 has been reported to be aberrantly expressed in diverse kinds of human malignancy. However, the function and underlying mechanisms of LINC00473 in glioma still remain unclear. In the present study, LINC00473 was notably elevated in glioma tissues and cell lines. High LINC00473 expression was associated with advanced WHO grade (III-IV), low Karnofsky performance score (KPS), and poor prognosis. Loss function assays showed that LINC00473 knockdown decreased glioma cell proliferation, invasion and epithelial-mesenchymal transition (EMT) processes , and reduced tumor growth . Mechanistic analysis indicated that LINC00473 regulated CDK6 expression by competitively binding to miR-637. Moreover, rescue assays revealed that miR-637 inhibitors abolished the effects of LINC00473 suppression on glioma cells progression. Thus, we demonstrated that LINC00473 could act as a ceRNA of miR-637 to promote glioma progression through regulating CDK6 expression, which provided a potential therapeutic target for treatment of glioma patients.
LINC00473 在多种人类恶性肿瘤中被报道存在异常表达。然而，LINC00473 在神经胶质瘤中的功能和潜在机制仍不清楚。在本研究中，LINC00473 在神经胶质瘤组织和细胞系中明显上调。高 LINC00473 表达与高级别 WHO 分级（III-IV）、低 Karnofsky 表现评分（KPS）和不良预后相关。功能丧失实验表明，LINC00473 敲低降低了神经胶质瘤细胞的增殖、侵袭和上皮-间充质转化（EMT）过程，并减少了肿瘤生长。机制分析表明，LINC00473 通过竞争性结合 miR-637 来调节 CDK6 的表达。此外，挽救实验表明，miR-637 抑制剂消除了 LINC00473 抑制对神经胶质瘤细胞进展的影响。因此，我们证明 LINC00473 可以作为 miR-637 的 ceRNA 通过调节 CDK6 的表达来促进神经胶质瘤的进展，为神经胶质瘤患者的治疗提供了一个潜在的治疗靶点。
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