ABSTRACT
BACKGROUND: LncRNA GAS8-AS1 inhibits thyroid carcinoma, but its function in other malignancies is unknown. The present study aimed to investigate the involvement of GAS8-AS1 in pancreatic cancer (PC). METHODS: The present study included 68 PC patients (38 males and 30 females, 42-66 years, 52.1 ± 4.5) and 62 healthy volunteers (28 males and 24 females, 43-67 years, 52.3 ± 4.9). Real-time quantitative PCR, transient cell transfection, and in vitro cell migration and invasion assays were applied for the research. RESULTS: The study showed that plasma GAS8-AS1 was lower in PC patients than in healthy controls. Downregulation of plasma GAS8-AS1 distinguished early-stage PC patients from healthy controls. Patients with low GAS8-AS1 plasma levels showed a significantly lower 5-year overall survival rate. Plasma miR-1179 levels were also significantly lower in PC patients than in healthy controls and were positively correlated with plasma GAS8-AS1 levels in PC patients but not healthy controls. GAS8-AS1 overexpression upregulated miR-1179, and MiR-1179 overexpression increased GAS8-AS1 level. Overexpression of both GAS8-AS1 and miR-1179 inhibited PC cell migration and invasion. CONCLUSION: GAS8-AS1 may promote PC by positively interacting with miR-1179.
Subject(s)
MicroRNAs , Pancreatic Neoplasms , RNA, Long Noncoding , Adult , Aged , Biomarkers , Cell Line, Tumor , Cell Movement/genetics , Cell Proliferation/genetics , Female , Gene Expression Regulation, Neoplastic , Humans , Male , MicroRNAs/genetics , Middle Aged , Pancreatic Neoplasms/diagnosis , Pancreatic Neoplasms/genetics , Prognosis , RNA, Long Noncoding/genetics , Pancreatic NeoplasmsABSTRACT
PURPOSE: Accumulating evidence indicates that genetic polymorphisms in ATP-binding cassette superfamily members, such asABCC2 and ABCG2, alter responses to antiepileptic drugs (AEDs); however, this evidence is controversial and inconclusive. To provide strong evidence of the association between common polymorphisms in ABCC2 and ABCG2 and AED responses in patients with epilepsy, we performed a systematic review and meta-analysis. METHODS: A literature search of electronic databases (PubMed, EBSCO, Ovid and the China National Knowledge Infrastructure) was performed. To evaluate the association of genetic polymorphisms inABCC2 and ABCG2 and risk of AED treatment, we calculated pooled odds ratios (ORs) and 95 % confidence intervals (CIs) using a fixed- or random-effect model. RESULTS: A significant association of theABCC2 rs717620 polymorphism with resistance to AEDs was found in the overall pooled populations (homozygous comparison: OR = 1.77, 95 % CI, 1.27-2.48; dominant model: OR = 1.23, 95 % CI, 1.06-1.43; recessive model: OR = 1.75, 95 % CI, 1.28-2.40) and Asians (dominant model: OR = 1.21, 95 % CI, 1.03-1.42; recessive model: OR = 1.80, 95 % CI, 1.30-2.50). Using a recessive model, a similarly significant association of ABCC2 rs3740066 with AED resistance was observed in the overall pooled populations (OR = 2.29, 95 % CI, 1.44-3.64) and Asians (OR = 2.53, 95 % CI, 1.56-4.08). However, ABCC2 rs2273697, ABCG2 rs2231137 and rs2231142 were not found to be associated with AED responsiveness. CONCLUSION: This meta-analysis suggests thatABCC2 rs717620 and rs3740066 are risk factors that predict responses to AEDs in epileptic patients.