Abstract
Non-small-cell lung cancer (NSCLC) is well established as one of the major subtypes of human lung cancer. NSCLC is characterized by a high incidence rate and poor patient prognosis. Previous studies have identified that long intergenic non-coding RNA (lincRNA) serves a key role in the development of tumor and malignant metastasis. However, the majority of the underlying mechanisms for lincRNA deregulation in various diseases, including cancer and diabetes, have not been completely elucidated. In the present study, the deregulation of lincRNA-p21 in NSCLC tumor tissues in comparison to adjacent healthy tissues was examined using reverse transcription-quantitative polymerase chain reaction. Furthermore, the effect of lincRNA-p21 overexpression and knockdown on different NSCLC cell lines was further investigated in vitro. The association between lincRNA-p21 expression and microRNA (miR)-17-5p level in NSCLC tumor cells was also investigated to clarify the underlying mechanism. The influence of miR-17-5p on different NSCLC cell lines A549 and PC9 were also examined in vitro using miR-17-5p mimics and inhibitors. Bioinformatics and luciferase assays were conducted to verify the direct binding sites on lincRNA-p21 for miR-17-5p. The results demonstrated that there was a significant low-expression of lincRNA-p21 in NSCLC tumor tissues, and lincRNA-p21 effectively inhibited the progression of lung cancer cells by suppressing cell proliferation and migration and promoting cell apoptosis. An evident negative association between lincRNA-p21 and miR-17-5p expression was observed, and the inhibitory effect of overexpressed lincRNA-p21 on lung cancer cells was counteracted by miR-17-5p. Bioinformatics and luciferase reporter analysis results confirmed that miR-17-5p is a direct target for lincRNA-p21. The present study provides evidence for lincRNA-p21 to inhibit the progression of NSCLC via direct targeting of a miR-17-5p associated signaling pathway.
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