In summary, our results showed that SM-inhibited NSCLC cell growth through the reciprocal interaction between HOTAIR and miR-214-3p, which ultimately suppressed PDPK1 gene expression.
Silencing of HOTAIR reduced EP4 protein levels and repressed the growth of NSCLC cells, while overexpression of HOTAIR and SP1 overcame XJD-reduced EP4 protein expression.
Thus, lncRNA-HOTAIR plays an important role in the occurrence and development of non-small cell lung cancer, and it may be an important factor in the clinical prognosis of patients with non-small cell lung cancer.
The targeting relationship between HOTAIR and miR-613 was first revealed by bioinformatics prediction. miR-613 was found to be lowly expressed in NSCLC tumor tissues and cell lines.
The lncRNAs HOTAIR, H19 and MALAT1 were up-regulated, while PANDAR and TUG1 were down-regulated in NSCLC cancer tissues compared with the corresponding adjacent normal tissue.
The ROC curves showed that plasma HOTAIR has high diagnostic accuracy for NSCLC, and the area under curve (AUC) for NSCLC versus healthy was 0.791 (95% CI: 0.727-0.855) which was higher than carcinoembryonic antigen (CEA) (AUC = 0.737, 95% CI: 0.666-0.808).
To the best of our knowledge, the present study provides the first <i>in vivo</i> and <i>in vitro</i> evidence to suggest that HOTAIR promotes the expression of 14-3-3σ in NSCLC.
Expression of HOTAIR was analyzed in 42 NSCLC tissues and four NSCLC cell lines by quantitative reverse-transcription polymerase chain reaction (qRT-PCR).
In this study, we examined the expression of HOTAIR in 77 NSCLCs, their corresponding normal lung tissues and 6 brain metastases by quantitative real-time RT-PCR.