长非编码 RNA LSINCT5 通过稳定 HMGA2 促进非小细胞肺癌的恶性转化。
The long non-coding RNA LSINCT5 promotes malignancy in non-small cell lung cancer by stabilizing HMGA2.
机构信息
a Department of Respiratory, Luoyang Central Hospital , Zhengzhou University , Luoyang , China.
出版信息
Cell Cycle. 2018;17(10):1188-1198. doi: 10.1080/15384101.2018.1467675. Epub 2018 Jul 5.
Abstract
Long non-coding RNAs (lncRNAs) can actively participate in tumorigenesis in various cancers. However, the involvement of lncRNA long stress induced non-coding transcripts 5 (LSINCT5) in non-small cell lung cancer (NSCLC) remains largely unknown. Here we showed a novel lncRNA signature in NSCLC through lncRNA profiling. Increased LSINCT5 expression positively correlates with malignant clinicopathological features and poor survival. LSINCT5 can promote migration and viability of various NSCLC cells in vitro and also enhance lung cancer progression in vivo. RNA immunoprecipitation followed by mass spectrometry has identified that LSINCT5 interacts with HMGA2. This physical interaction can increase the stability of HMGA2 by inhibiting proteasome-mediated degradation. Therefore, LSINCT5 may possibly contribute to NSCLC tumorigenesis by stabilizing the oncogenic factor of HMGA2. This novel LSINCT5/HMGA2 axis can modulate lung cancer progression and might be a promising target for pharmacological intervention.
摘要
长链非编码 RNA（lncRNA）可以在各种癌症中积极参与肿瘤发生。然而，长链非编码 RNA 长应激诱导非编码转录物 5（LSINCT5）在非小细胞肺癌（NSCLC）中的参与仍然很大程度上未知。在这里，我们通过 lncRNA 分析显示了 NSCLC 中的一个新的 lncRNA 特征。LSINCT5 表达增加与恶性临床病理特征和不良预后呈正相关。LSINCT5 可以促进各种 NSCLC 细胞在体外的迁移和活力，并增强体内肺癌的进展。RNA 免疫沉淀结合质谱分析已经确定 LSINCT5 与 HMGA2 相互作用。这种物理相互作用可以通过抑制蛋白酶体介导的降解来增加 HMGA2 的稳定性。因此，LSINCT5 可能通过稳定致癌因子 HMGA2 来促进 NSCLC 的肿瘤发生。这个新的 LSINCT5/HMGA2 轴可以调节肺癌的进展，可能是药物干预的一个有前途的靶点。
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