[No authors listed]
OBJECTIVE:Previous studies have shown the carcinogenic role of long-chain non-coding RNAs (lncRNA) However, the role of in non-small cell lung cancer (NSCLC) has not been reported. This research aims to explore the regulatory effect of axis on the malignant progression of NSCLC. PATIENTS AND METHODS:Quantitative Real (qRT-PCR) was performed to examine the expression levels of Tduanyu1795NA1 and FOXL1 in 39 pairs of tumor tissues and paracancerous ones collected from NSCLC patients. The potential relation between Tduanyu1795NA1 expression and clinical indicators of NSCLC patients was analyzed. Meanwhile, expression levels of Tduanyu1795NA1 and FOXL1 in NSCLC cell lines were also detected by qRT-PCR. In addition, Tduanyu1795NA1 knockdown model was constructed in H358 and SPC-A1 cells. Cell counting kit-8 (CCK-8), cell colony formation assay, and flow cytometry were applied to analyze the influence of Tduanyu1795NA1 on NSCLC cell biological functions. Finally, Dual-Luciferase reporter gene assay and cell reverse recovery experiments were performed to figure out the underlying mechanisms of Tduanyu1795NA1 in regulating NSCLC progression. RESULTS:QRT-PCR results indicated that the expression level of lncRNA Tduanyu1795NA1 in tumor tissue samples of NSCLC patients was remarkably higher than that in adjacent tissues. Compared with NSCLC patients with low expression of patients with high Tduanyu1795NA1 expression had a worse pathological stage and overall survival. Similarly, compared with cells in sh-NC group, the proliferation ability of cells in group was remarkably attenuated. In addition, cell ratio in the G1 phase increased after knockdown of Tduanyu1795NA1, suggesting the arrested G1/S cell cycle. Subsequently, FOXL1 was downregulated in NSCLC cell lines and tumor tissues. Meanwhile, FOXL1 level was verified to be negatively correlated with Tduanyu1795NA1 level. Additionally, the binding between Tduanyu1795NA1 and FOXL1 was confirmed by Dual-Luciferase reporter gene assay. Cell reverse investigation indicated the involvement of FOXL1 in malignant progression of NSCLC. CONCLUSIONS:LncRNA Tduanyu1795NA1 was up-regulated both in NSCLC tissues and cell lines. Its level was associated with pathological stage and poor prognosis in NSCLC. In addition, lncRNA Tduanyu1795NA1 could promote the malignant progression of NSCLC via modulating FOXL1.
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