Long non-coding RNA ASAP1-IT1 promotes cell proliferation, invasion and metastasis through the PTEN/AKT signaling axis in non-small cell lung cancer.

OBJECTIVE To investigate the relative expression of long non-coding RNA (lncRNA) ASAP1-IT1 (hereafter called ASAP1-IT1) in tissues and cells of non-small cell lung cancer (NSCLC) patients, so as to explore the effect of ASAP1-IT1 on the biological effect of NSCLC cells. PATIENTS AND METHODS Real-time quantitative polymerase chain reaction (qRT-PCR) was performed to detect the relative expressions of ASAP1-IT1 on tissues of 68 NSCLC patients and 5 cell lines. Besides, the interference sequence of ASAP1-IT1 was designed to detect the transfection efficiency through qRT-PCR experiment. Cell count kit 8 (CCK-8) and clone formation experiment were also carried out to determine the effect of ASAP1-IT1 expression under interference on the proliferation ability of NSCLC cells. In addition, transwell experiment was also performed to investigate the effects of ASAP1-IT1 expression under interference on the invasion and metastasis of NSCLC cells. Furthermore, the Western blotting assay was also conducted to detect the downstream signal pathways through which ASAP1-IT1 regulated the biological behaviors of NSCLC. RESULTS The results of qRT-PCR experiment showed that in 68 NSCLC samples, upregulation of ASAP1-IT1 expression was identified in 51 samples (82.4%) in comparison with the expression in tumor-adjacent tissues, and a similar upregulation was also observed in 5 NSCLC cells. CCK-8 and clone formation experiments also revealed that interference on ASAP1-IT1 expression could inhibit the proliferation of NSCLC cells, while the transwell experiment showed that the interference on ASAP1-IT1 expression could block the migration and invasion ability of NSCLC cells. The results of Western blotting assay also indicated that ASAP1-IT1 could regulate the biological behaviors of NSCLC cells through phosphatase and tensin homolog deleted on chromosome ten (PTEN)/serine-threonine kinase (AKT) pathway. CONCLUSIONS In this study, it was found that the expression of ASAP1-IT1 is relatively upregulated in NSCLC cells and tissues, which can promote the proliferation, invasion and metastasis of NSCLC cells through regulating the PTEN/AKT signal pathway. Thus, the therapeutic target of ASAP1-IT1 is expected to provide important ideas for reversing the malignant phenotype of NSCLC in clinical practice.