Department of Emergency, Part 2 of the First Hospital, Jilin University, Changchun, China.
Department of Oncology and Hematology, China-Japan Union Hospital of Jilin University, Changchun, China.
J Cell Physiol. 2019 Aug;234(8):13843-13850. doi: 10.1002/jcp.28064. Epub 2019 Jan 7.
Lung cancer belongs to a leading popular and malignant cancer around the world. However, the root mechanism underlying lung cancer progression remains unclear. Recently, long noncoding RNA (lncRNA) has been identified as important for tumorigenesis. LncRNA MNX1-AS1 is proven to regulate colon adenocarcinoma, cervical cancer, glioblastoma, and ovarian cancer. Whether MNX1-AS1 participates in lung cancer needs investigation. In our research, we found that MNX1-AS1 was dramatically upregulated in lung cancer. MNX1-AS1 upregulation indicated poor prognosis in lung cancer patients. Functionally, MNX1-AS1 promoted lung cancer progression through regulating proliferation, migration, and invasion. Mechanistically, MNX1-AS1 was found to locate in the cytoplasm and interact with miR-527. Through inhibiting miR-527 availability, MNX1-AS1 facilitated BRF2 expression. Restoration of BRF2 rescued defects of proliferation, migration, and invasion caused by MNX1-AS1 knockdown. Taken together, our study found a novel signaling pathway, namely MNX1-AS1/miR-527/BRF2 axis, involved in lung cancer progression.
肺癌属于全球范围内一种主要的流行和恶性癌症。然而，肺癌进展的根本机制仍不清楚。最近，长非编码 RNA（lncRNA）已被确定对肿瘤发生具有重要作用。lncRNA MNX1-AS1 已被证明可调节结肠癌、宫颈癌、胶质母细胞瘤和卵巢癌。MNX1-AS1 是否参与肺癌需要进一步研究。在我们的研究中，发现 MNX1-AS1 在肺癌中显著上调。MNX1-AS1 的上调预示着肺癌患者的预后不良。功能上，MNX1-AS1 通过调节增殖、迁移和侵袭促进肺癌进展。机制上，发现 MNX1-AS1 位于细胞质中并与 miR-527 相互作用。通过抑制 miR-527 的可用性，MNX1-AS1 促进 BRF2 的表达。BRF2 的恢复挽救了 MNX1-AS1 敲低引起的增殖、迁移和侵袭缺陷。总之，我们的研究发现了一个新的信号通路，即 MNX1-AS1/miR-527/BRF2 轴，参与肺癌的进展。
