Background
Lung cancer is one of the most common human cancers. Long noncoding RNA-activated by DNA damage (NORAD) is often upregulated and promotes cell progression in various human cancers; however, its function and possible mechanism in lung cancer remain largely unknown.
Conclusion
NORAD knockdown suppressed cell proliferation, migration and invasion but promoted cell apoptosis in lung cancer cells by regulating miR-30a-5p/ADAM19, providing a possible therapeutic strategy for lung cancer patients.
Methods
The expression levels of NORAD, miR-30a-5p and a disintegrin and metalloproteinase 19 (ADAM19) were evaluated by quantitative real-time polymerase chain reaction (qRT-PCR). 3-(4, 5)-dimethylthiazole-2-y1)-2, 5-biphenyl tetrazolium bromide (MTT) assay, flow cytometry, and transwell assay were employed to detect cell proliferation, apoptosis, migration, and invasion abilities, respectively. Western blot was used to detect the protein expression of ADAM19. The interaction between miR-30a-5p and NORAD or ADAM19 was predicted by online software and confirmed by the dual-luciferase reporter assay.
Results
The expression levels of NORAD and ADAM19 were increased and the expression level of miR-30a-5p was decreased in lung cancer tissues and cells. Knockdown of NORAD could inhibit cell proliferation, migration and invasion but promote apoptosis in lung cancer cells. In addition, NORAD directly interacted with miR-30a-5p and its overexpression reversed the anti-cancer role of miR-30a-5p in lung cancer. Moreover, miR-30a-5p directly targeted ADAM19 and its inhibition attenuated the inhibitory effect of ADAM19 knockdown on progression of lung cancer cells. Furthermore, NORAD functioned as a competing endogenous RNA (ceRNA) through sponging miR-30a-5p to regulate ADAM19 expression.