Department of Thoracic and Cardiovascular Surgery, The Second Affiliated Hospital of Guangxi Medical University, No.166 Da Xuedong Road, Nanning City, Guangxi Province, 530007, People's Republic of China.
BMC Pulm Med. 2021 Feb 3;21(1):50. doi: 10.1186/s12890-020-01369-3.
LINC01116 is a recently identified oncogenic lncRNA in glioma. Differential expression analysis using the public gene expression analysis tool GEPIA revealed the upregulation of LINC01116 in lung cancer. We studied the functions of LINC01116 in small cell lung cancer (SCLC).
The expression of LINC01116 in several types of cancer tissue and the paired non-tumor tissues was evaluated by GEPIA. The effects of the overexpression of LINC01116 and miR-93-5p on the expression of STAT3 were evaluated. The effects of the overexpression of LINC01116, miR-93-5p and STAT3 on SHP-77 cell behaviors were evaluated by Transwell assays.
LINC01116 was highly expressed in SCLC and predicted poor survival. In SCLC tissues, the expression of LINC01116 was positively correlated with STAT3. Bioinformatics analysis revealed that miR-93-5p may target LINC01116. Overexpression of LINC01116 increased STAT3 but did not affect the expression of miR-93-5p. Transwell assay showed that LINC01116 and STAT3 increased cell invasion and migration rates. MiR-93-5p played an suppressed cell behaviors and suppressed the role of LINC01116.
Therefore, LINC01116 might upregulate STA3 by sponging miR-93-5p, thereby promoting cell invasion and migration in SCLC.
LINC01116 是一种新发现的脑胶质瘤致癌 lncRNA。使用公共基因表达分析工具 GEPIA 进行差异表达分析显示,LINC01116 在肺癌中上调。我们研究了 LINC01116 在小细胞肺癌(SCLC)中的功能。
通过 GEPIA 评估了几种类型的癌组织和配对的非肿瘤组织中 LINC01116 的表达。评估了过表达 LINC01116 和 miR-93-5p 对 STAT3 表达的影响。通过 Transwell 测定评估了过表达 LINC01116、miR-93-5p 和 STAT3 对 SHP-77 细胞行为的影响。
LINC01116 在 SCLC 中高表达,预测预后不良。在 SCLC 组织中,LINC01116 的表达与 STAT3 呈正相关。生物信息学分析显示,miR-93-5p 可能靶向 LINC01116。过表达 LINC01116 增加了 STAT3,但不影响 miR-93-5p 的表达。Transwell 测定显示,LINC01116 和 STAT3 增加了细胞侵袭和迁移率。miR-93-5p 发挥抑制细胞行为的作用,并抑制 LINC01116 的作用。
因此,LINC01116 可能通过海绵吸附 miR-93-5p 而上调 STAT3,从而促进 SCLC 中的细胞侵袭和迁移。