Conclusion
Our findings suggested that LINC00472 contributed to the increase in lung adenocarcinoma cell apoptosis and the inhibition of proliferation via regulating miR-24-3p/ DEDD, which might provide a novel insight into potential therapeutic approach for lung adenocarcinoma.
Methods
Long noncoding RNA, microRNA, and messenger RNA levels were determined using reverse transcription quantitative polymerase chain reaction. The expression of death effector domain-containing DNA-binding protein was determined using Western blot assay. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and colony formation assay were conducted to explore the proliferation of cells. The cell apoptosis was tested by flow cytometry assay. Target relationships between miR-24-3p, death effector domain-containing DNA-binding protein, and LINC00472 were validated by dual-luciferase reporter gene assay.
Objective
We aimed to detect the role of LINC00472 via regulating miR-24-3p and death effector domain-containing DNA-binding protein in lung adenocarcinoma.
Results
LINC00472 and death effector domain-containing DNA-binding protein were found to be underexpressed, whereas miR-24-3p was found overexpressed in lung adenocarcinoma cell lines and tissues. Both LINC00472 and death effector domain-containing DNA-binding protein can bind to miR-24-3p. Overexpression of LINC00472 led to higher death effector domain-containing DNA-binding protein level, demoting cell proliferation while promoting apoptosis. Overexpression of miR-24-3p reduced death effector domain-containing DNA-binding protein level, which facilitated cell proliferation and inhibited cell apoptosis, as well as to some extent restrained the effects of LINC00472. The high expression of miR-24-3p in tumor cells was negatively related to LINC00472 and death effector domain-containing DNA-binding protein, whereas the expression of LINC00472 and that of death effector domain-containing DNA-binding protein were positively correlated.