KCNQ1OT1 通过调节 miRNA-27b-3p/HSP90AA1 轴促进非小细胞肺癌的进展。
KCNQ1OT1 facilitates progression of non-small-cell lung carcinoma via modulating miRNA-27b-3p/HSP90AA1 axis.
机构信息
Department of Laboratory Medicine, Shanghai Sixth People's Hospital Jinshan Branch, Shanghai, China.
Fangsong Community Health Centre, Shanghai, China.
出版信息
J Cell Physiol. 2019 Jul;234(7):11304-11314. doi: 10.1002/jcp.27788. Epub 2018 Nov 23.
Long noncoding RNA KCNQ1OT1 participates in the regulation of imprinted genes within the kcnq1 domain. But its roles in carcinogenesis and metastasis remain largely elusive. Herein, we evaluated its potential in non-small-cell lung cancer (NSCLC) progression. We demonstrated that the KCNQ1OT1 level was upregulated in NSCLC tissues and cell lines. High KCNQ1OT1 level correlated with poor overall and progression-free survival in NSCLC patients. KCNQ1OT1 facilitated proliferation, migration, and invasion in H460 cells. Furthermore, knockdown of KCNQ1OT1 reduced the expression of HSP90AA1. KCNQ1OT1 presented a positive correlation with HSP90AA1 which predicted the tumor progression in NSCLC from The Cancer Genome Atlas database. Intriguingly, KCNQ1OT1 modulated HSP90AA1 expression by sponging miR-27b-3p. MiR-27b-3p counteracted the effect of KCNQ1OT1 on HSP90AA1 expression, H460 cell migration, and invasion. These data revealed a role for KCNQ1OT1 as an oncogene through miR-27b-3p/HSP90AA1 axis during NSCLC progression.
长链非编码 RNA KCNQ1OT1 参与印迹基因在 kcnq1 域内的调控。但其在致癌和转移中的作用仍很大程度上难以捉摸。在此，我们评估了其在非小细胞肺癌（NSCLC）进展中的潜力。我们证明 KCNQ1OT1 水平在 NSCLC 组织和细胞系中上调。高水平的 KCNQ1OT1 与 NSCLC 患者的总生存期和无进展生存期不良相关。KCNQ1OT1 促进 H460 细胞的增殖、迁移和侵袭。此外，KCNQ1OT1 的敲低降低了 HSP90AA1 的表达。KCNQ1OT1 与 HSP90AA1 呈正相关，这从癌症基因组图谱数据库预测了 NSCLC 的肿瘤进展。有趣的是，KCNQ1OT1 通过海绵 miR-27b-3p 调节 HSP90AA1 的表达。miR-27b-3p 抵消了 KCNQ1OT1 对 HSP90AA1 表达、H460 细胞迁移和侵袭的影响。这些数据揭示了 KCNQ1OT1 通过 miR-27b-3p/HSP90AA1 轴在 NSCLC 进展过程中作为癌基因的作用。
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