4.4 Article

Circ-IGF1R inhibits cell invasion and migration in non-small cell lung cancer

期刊

THORACIC CANCER
卷 11, 期 4, 页码 875-887

出版社

WILEY
DOI: 10.1111/1759-7714.13329

关键词

Circ-IGF1R; circular RNA; invasion; migration; NSCLC

资金

  1. National Natural Science Foundation of China [NSFC81660488]
  2. Guangxi Nat-ural Science Foundation [2017GXNSFAA198123]

向作者/读者索取更多资源

Background Circular RNA (circRNA) is a novel molecular marker and target candidate that is closely associated with tumor invasion and migration. The mechanism of action of hsa_circ_0005035 (circ-IGF1R) in non-small cell lung cancer remains unclear. In this study, we aimed to study the mechanism of action of circ-IGF1R in lung cancer. Methods We screened circ-IGF1R, one of the most notable differential expressions, from the Gene Expression Omnibus database, GSE104854, for further research. The expression level of circ-IGF1R was examined using quantitative reverse transcription-polymerase chain reaction (qRT-PCR) in five different lung cancer cell lines and 50 pairs of lung cancer and adjacent tissues. Wound-healing and Transwell assays were used for verifying the biological function of circ-IGF1R. The effect of overexpressing circ-IGF1R on the transcriptome of whole lung cancer cells was explored in lung cancer cell lines using RNA-seq. Results The expression level of circ-IGF1R was notably lower in lung cancer tissues and lung cancer cell lines than in the adjacent normal tissues and cells (P < 0.0001). In addition, the expression level of circ-IGF1R was associated with larger tumors (T2/T3/T4) and lymph node metastasis (N1/ N2/N3) (P < 0.05). The overexpression of circ-IGF1R significantly inhibited the invasion and migration of the lung cancer cells. The potential network of circ-IGF1R-miR-1270-VANGL2 was preliminarily determined, and the expression patterns of miR-1270 and VANGL2 were verified in lung cancer cell lines. Conclusion Circ-IGF1R may inhibit lung cancer invasion and migration through a potential network of circ-IGF1R-miR-1270-VANGL2.

作者

我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。

评论

主要评分

4.4
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

暂无数据
暂无数据