RETRACTED: Long Noncoding RNA LINC00472 Inhibits Proliferation and Promotes Apoptosis of Lung Adenocarcinoma Cells via Regulating miR-24-3p/DEDD

Abstract

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.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.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.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.

Peer Review #2 of "Comprehensive analysis of lncRNA-associated competing endogenous RNA network in tongue squamous cell carcinoma (v0.2)"

“…Notably, decreased expression of LINC00261 indicated a better prognosis in TSCC. Our study found LINC00261 regulated the expression of ENPP4 and ENPP5, however, these two genes have not been Several existing studies indicate that LINC00472 plays an important role in inhibiting tumor development (Shen et al 2015;Su et al 2018;Ye et al 2018). Our study also showed the similar results that higher expression of LINC00472 was associated with better prognosis.…”

Comprehensive analysis of lncRNA-associated competing endogenous RNA network in tongue squamous cell carcinoma

“…Several existing studies indicate that LINC00472 plays an important role in inhibiting tumor development (Shen et al, 2015; Su et al, 2018; Ye et al, 2018). Our study also showed the similar results that higher expression of LINC00472 was associated with better prognosis.…”

MicroRNA-24-3p regulates neuronal differentiation by controlling hippocalcin expression

“…Thus far, most research on miR - 24 - 3p has focused on its function in cancer using in vitro model systems. For instance, up or downregulation of miR - 24 is important for regulation of the growth and/or apoptosis of various cancer types, including breast cancer [40], lung adenocarcinoma [41], hepatocellular carcinoma [42], and colon cancer [43]. In the present study, we investigated its function in neuronal differentiation.…”