Abstract
Objective: This study presents a discussion regarding the mechanism affecting the malignant progression of LUAD and the potential therapeutic targets, so as to provide more effective therapeutic strategies for LUAD patients.
Methods: Expression data from TCGA-LUAD were extracted to identify target miRNA, with its downstream target mRNA predicted using bioinformatics analysis. Gene expression in transcript level and protein level were separately examined by qRT-PCR and western blot. Cell malignant phenotypes were assessed via MTT and Transwell assays. Luciferase reporter plasmids carrying target gene sequences were constructed to verify the targeting association between the target miRNA and its downstream mRNA.
Results: miR-1-3p showed decreased expression in LUAD. Over-expressing miR-1-3p suppressed cancer cells to proliferate, migrate and invade. CELSR3, directly regulated by miR-1-3p, presented significantly elevated expression in LUAD and could foster LUAD cells to proliferate, migrate and invade. The rescue experiment identified that miR-1-3p-induced inhibition on LUAD cell malignant phenotypes could be reversed by over-expressing CELSR3.
Conclusion: This study uncovered that miR-1-3p could suppress the malignant phenotypes of LUAD cells by targeting CELSR3, which will help to provide novel therapeutic strategies for LUAD sufferers and new references for the targeted therapy of LUAD.
Keywords: Lung adenocarcinoma, miR-1-3p, CELSR3, proliferation, migration, invasion.
Graphical Abstract