Department of Thoracic Surgery, Shanghai Chest Hospital, Shanghai Jiaotong University, Shanghai, P. R. China.
Outpatient Department, Hunan Provincial People's Hospital, The First Affiliated Hospital of Hunan Normal University, Changsha, P. R. China.
Am J Pathol. 2020 Jun;190(6):1343-1354. doi: 10.1016/j.ajpath.2020.02.011. Epub 2020 Mar 20.
Lung adenocarcinoma (LUAD) is a malignant tumor with poor patient survival and high patient mortality. Long noncoding RNA is profoundly involved in the tumorigenesis of LUAD. The present study explores the effect of small nucleolar RNA host gene 7 (SNHG7) on the progression of LUAD and its underlying mechanisms. SNHG7 was found to be down-regulated in LUAD tissues compared with normal tissues. Altered SNHG7 expression induced changes in cell proliferation and migration both in vitro and in vivo. Mechanistically, it was found that SNHG7 interacted with microRNA mir-181 and sequentially up-regulated cbx7. cbx7, which suppresses the Wnt/β-catenin pathway in LUAD, was found to be a direct target of mir-181. Taken together, loss of SNHG7 in LUAD up-regulated mir-181 and then down-regulated the tumor suppressor cbx7.
肺腺癌 (LUAD) 是一种恶性肿瘤,患者的生存率和死亡率都很高。长链非编码 RNA 深刻参与 LUAD 的肿瘤发生。本研究探讨了小核仁 RNA 宿主基因 7 (SNHG7) 对 LUAD 进展的影响及其潜在机制。与正常组织相比,LUAD 组织中 SNHG7 的表达下调。改变 SNHG7 的表达在体外和体内均诱导细胞增殖和迁移的变化。在机制上,发现 SNHG7 与 microRNA mir-181 相互作用,并顺式上调 cbx7。抑制 LUAD 中 Wnt/β-catenin 通路的 cbx7 被发现是 mir-181 的直接靶标。总之,LUAD 中 SNHG7 的缺失上调了 mir-181,进而下调了肿瘤抑制因子 cbx7。