[Effect of long non-coding RNA MBNL1-AS1 expression on prognosis of acute myeloid leukemia patients].

Objective: To explore the prognosis effect of the expression of long-chain non-coding RNA (lncRNA) MBNL1-AS1 on acute myeloid leukemia (AML) patients. Methods: One hundred and twenty-five AML patients of the Cancer Genome Atlas (TCGA) from November 2001 to March 2010 were involved, including 70 patients who received chemotherapy only and other 55 patients treated with allogeneic hematopoietic stem cell transplantation (allo-HSCT) in addition to chemotherapy. According to the median expression of lncRNA MBNL1-AS1, patients of chemotherapy group were divided into high expression sub-group(n=35) and low expression sub-group (n=35), and patients of allo-HSCT group were also divided into high expression sub-group (n=28) and low expression sub-group (n=27) for prognosis analysis. Clinical characteristics at diagnosis, including peripheral white blood cell counts (WBC), blast percentages in peripheral blood and bone marrow (BM), French-American-British (FAB) subtypes and the frequencies of common genetic mutations in AML were described. The event-free survival (EFS) rate and overall survival (OS) rate of patients in different groups were analyzed, and the influence of the clinical characteristics of patients on the prognosis of AML was analyzed by COX multivariate analysis. Results: In the chemotherapy group, patients with low lncRNA-MBNL1-AS1 expression had significantly lower EFS and OS (60.0%, 8.6%) than patients with high lncRNA-MBNL1-AS1 expression (68.6%, 34.3%) (χ²=7.817, 10.880, all P<0.01). However, in the alloHSCT group, no significant differences were observed in EFS and OS of patients between high and low expression groups of lncRNA-MBNL1-AS1 (all P>0.05). COX multivariate analysis confirmed that age≥60 years old (EFS: HR (95%CI): 6.934 (1.918-25.075),P=0.003;OS: HR (95%CI): 4.119 (1.812-9.364), P=0.001), and low expression of lncRNA MBNL1-AS1 (EFS: HR (95%CI): 0.354 (0.126-0.941), P=0.038; OS: HR (95%CI): 0.424 (0.231-0.778), P=0.006)were independent risk factors for EFS and OS in the chemotherapy group. Conclusion: The long-chain non-coding RNA MBNL1-AS1 is related to the prognosis of AML, and its low expression is an independent poor prognostic factor in AML patients.

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.