Abstract
The morbidity of lung cancer ranks first among all cancers. Lung adenocarcinoma (LUAD) is a classification of lung cancer, and cell invasion and migration of LUAD are the main causes for its high mortality. Therefore, further exploring the potential mechanism of LUAD metastasis may provide bases for following targeted drug development and treatment of LUAD. In this study, clinical data as well as gene expression profiles were obtained from TCGA-LUAD and GEO to analyze CTHRC1 expression. The result found that CTHRC1 was significantly high in LUAD. Similar results were also discovered in 4 cancer cell lines. Moreover, overexpressed/knock-down CTHRC1 cell lines were constructed. It was uncovered that overexpressing CTHRC1 promoted LUAD cell migration and invasion, and inhibited cell adhesion, while knocked down CTHRC1 had the opposite effect. Afterward, the upstream miRNAs that regulated CTHRC1 were predicted by several bioinformatics websites. It was testified by dual-luciferase method that CTHRC1 was negatively mediated by miR-30a-5p. Overexpressed miR-30a-5p suppressed cell invasion/migration, and increased cell adhesion, while overexpressing CTHRC1 as well reversed such impacts. In conclusion, it was disclosed in this study that CTHRC1 worked as a cancer promoter in LUAD, and miR-30a-5p could target and downregulate CTHRC1 to regulate cell adhesion, and inhibited LUAD cell invasion and migration. These results elucidated at cellular level that upregulated CTHRC1 may be a marker protein for LUAD metastasis.