OBJECTIVE: To detect the expressions of long intergenic non-protein coding ribonucleic acid 1638 (LINC01638) in non-small cell lung cancer (NSCLC) tissues and cells, and to explore the biological function of LINC01638 and the underlying mechanism of its high expression. PATIENTS AND METHODS: The relative expression levels of LINC01638 in NSCLC tissues and cells were determined via quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR). The interference sequences of LINC01638 were designed, and the interference efficiency was measured using qRT-PCR. The influences of the interference in LINC01638 expression on the proliferation ability, the cycle distribution and apoptosis of NSCLC cells were detected via cell counting kit (CCK)-8 assay and flow cytometry. The changes in the expressions of the molecular markers in the downstream Phosphatase and Tensin Homolog deleted on chromosome ten (PTEN)/protein kinase B (AKT) signaling pathway of LINC01638 were evaluated via Western blotting. Moreover, the upstream transcription factors of LINC01638 were predicted based on bioinformatics, and the expression of LINC01638 was detected via qRT-PCR after interfering in the expression of specificity protein 1 (SP1). RESULTS: According to the qRT-PCR results, the expression of LINC01638 was up-regulated in the NSCLC tissues and cells. After interference in LINC01638 expression, the cell proliferation ability was weakened according to the CCK-8 assay results. The flow cytometry results revealed that the cell cycle was arrested in G0/ G1 phase, while the apoptosis rate raised. It was found in the Western blotting that the expressions of the molecular markers in the PTEN/ AKT signaling pathway were altered. Additionally, the bioinformatics prediction results revealed that the transcription factor SP1 stimulated LINC01638 expression and that it was lowered after interfering in the expression of SP1. CONCLUSIONS: The expression of LINC01638 is upregulated in NSCLC tissues and cells, and the highly expressed LINC01638 is modulated by the transcription factor SP1 and promotes the proliferation but represses the apoptosis of NSCLC cells via the PTEN/AKT signaling pathway.
|Number of pages||8|
|Journal||European Review for Medical and Pharmacological Sciences|
|Publication status||Published - 2019|
- Non-small cell lung cancer
ASJC Scopus subject areas
- Pharmacology (medical)