The present study intended to demonstrate the effects of long noncoding RNA growth arrest-specific transcript 5 (GAS5) on the migration and invasion of melanoma cells. We first detected the expression of GAS5 among four kinds of melanoma cell lines, followed by constructing GAS5-knocked down and overexpressed stable cells. Next, we evaluated the effects of GAS5 on cell migration and invasion using wound healing and gelatin zymography assays. Finally, melanoma cells with different GAS5 expression were injected into nude mice, and the tumor volumes were recorded and tumor tissues were analyzed after sacrificing the mice. This study systematically examined the function of GAS5 in mediating melanoma metastasis and revealed that GAS5 plays an anticancer role in melanoma via regulating gelatinase A and B, both in vitro and in vivo.

Abstract. The present study evaluated the effects of long non-coding RNA GAS5 on the migration and invasion of melanoma cells. Using the SK-Mel-110 melanoma cell line, we stably expressed GAS5, visualized the distribution of GAS5 by RNA fluorescence in situ hybridization (FISH) and examined changes in cell migration and invasion with Transwell assays. In GAS5 overexpressed SK-Mel-110 cells, migrated and invaded cells decreased by 65.3 and 55.6%, respectively. Moreover, the MMP2 protein level, and its activity was downregulated by 67.9 and 15.8%, respectively. Overexpressing lncRNA GAS5 inhibited the migration and invasion ability of melanoma SK-Mel-110 cells, partially by decreasing the MMP2 expression and its activity. This study is the first to reveal a potential relationship between lncRNA GAS5 and the migration and invasion of melanoma.

Background. Trials on assessing the benefits of EGFR inhibitors in head and neck squamous cell carcinoma (HNSCC) patients have gradually been published. Nevertheless, the benefits of gefitinib in advanced HNSCC are still unknown. Methods. The Cochrane library, PubMed, and EMBASE databases were systematically searched from the inception dates to 17 July 2017, 18 July 2017, and 19 July 2017, respectively. The keywords “head and neck” and gefitinib were used to retrieve in articles and abstracts. An additional search for recently published randomized trials was performed from July 17, 2017, to April 18, 2018. Then we assessed the risk of bias of the included studies based on the Cochrane “Risk of Bias” tool. Quantitative analysis was carried out to evaluate the overall survival (OS), progression free survival (PFS), overall response rate (ORR), and grade 3-4 adverse effects by Review Manager 5.0.2 and the quality-of-life was analyzed in the included studies. Results. Seven randomized controlled trials and a total number of 1287 patients were involved. There were no significant differences in OS, PFS, or ORR between gefitinib and no gefitinib group (HR 1.07, 95% CI 0.93 to 1.22, and P=0.35; HR 0.84, 95% CI 0.69 to 1.04, and P=0.11; RR 1.04, 95% CI 0.90 to 1.20, and P =0.60, respectively). However, gefitinib alone was equivalent to chemotherapeutics (i.e., methotrexate; methotrexate + fluorouracil) in ORR in patients with recurrent HNSCC, and a trend of improvement in QOL in gefitinib group was showed. Toxicities revealed no differences except for diarrhea and skin toxicity (p=0.0003; p=0.03, respectively). Conclusion. For patients with advanced HNSCC, gefitinib cannot prolong the OS and PFS or improve ORR, and odds of skin toxicity and diarrhea increased. However, gefitinib alone is equivalent to methotrexate or methotrexate + fluorouracil and tends to improve QOL for recurrent patients.

[ 18 F]fluoro-2-deoxyglucose (FDG) positron emission tomography (PET)-computed tomography (CT) is a functional imaging modality based on glucose metabolism. The association between the maximum standardized uptake value (SUV max) from 18 F-FDG PET-CT scanning and epidermal growth factor receptor (EGFR) mutation status has, to the best of our knowledge, not previously been fully elucidated, and the potential mechanisms by which EGFR mutations alter FDG uptake are largely unknown. A total of 157 patients who were pathologically diagnosed with non-small cell lung cancer (NSCLC) who underwent EGFR mutation testing and PET-CT pretreatment between June 2015 and October 2017 were retrospectively analyzed. χ 2 and univariate analyses were performed to identify the contributors to EGFR mutation. The receiver operating characteristic (ROC) curve was analyzed, and the area under the curve (AUC) was calculated. Glucose transporter 1 (GLUT1) and NADPH oxidase 4 (NOX4) expression, and reactive oxygen species (ROS) activity were detected in the A549 (wild-type), PC-9 (EGFR mutation-positive, EGFR exon 19del) and NCI-H1975 (EGFR mutation-positive, combined with L858R and T790M substitution) cell lines. A total of 109 patients who met the criteria were enrolled, and 63 of those tested as EGFR mutation-positive. The SUV max values were significantly lower in patients with EGFR mutations (mean, 6.52±0.38) compared with in patients with wild-type EGFR (mean, 9.37±0.31; P<0.001). Using univariate analysis, EGFR mutation status was significantly associated with sex, smoking status, tumor histology and SUV max of the primary tumor. In the multivariate analysis, smoking status (never-smoking), histopathology (adenocarcinoma) and SUV max (≤9.91) were the statistically significant predictors of EGFR mutations. ROC curve analysis identified that the SUV max cutoff point was 9.92, for which the AUC was 0.75 (95% confidence interval, 0.68-0.83). Reverse transcription-polymerase chain reaction indicated that the GLUT1 mRNA decreased in the PC-9 and NCI-H1975 cell lines compared with the A549 cell line (0.82±0.07 and 0.72±0.04 vs. 0.98±0.04, respectively; P<0.05) and decreased ROS activity was observed in the PC-9 cell line. Furthermore, the expression of NOX4 mRNA decreased by 20% in PC-9 (P<0.01) and by 14% (P<0.05) in NCI-H1975 cells. In addition, NOX4 protein expression decreased by 13% in PC-9 and by 16% in NCI-H1975 cells (both P<0.05) compared with the A549 cell line. The SUV max could be considered to effectively predict EGFR mutation status of patients with NSCLC, and the EGFR mutation status may alter FDG uptake partially via the NOX4/ROS/GLUT1 axis.

Objective: The aim of this study was to evaluate the effect of acupuncture injection therapy for the patients with nonspecific chronic low back pain (CLBP) systematically. Methods: Four English online databases and 4 Chinese online databases will be researched systematically from their inception to December 31, 2018. Reference management software, Endnote X7, will be used to manage and screen the records. After removing the duplicate records, 2 independent reviewers will select the studies that meet the inclusion criteria. “Risk of table” recommend by Cochrane Handbook for Systematic Reviews of Interventions will be used to judge the quality of the included records. All data will be extracted by 1 reviewer and checked by another reviewer. Any disagree will be addressed via consulting a third reviewer in the above processes. Microsoft Excel will be used to manage and convert data if necessary. The missing data will be obtained via emailing the original authors of included studies. Review Manager (RevMan5.3) will be used to perform the data synthesis if enough data were collected. Otherwise, only the qualitative analysis will be performed. Based on the heterogeneity results, fixed-effect model or random-effect model will be used to estimate the overall effect of acupuncture injection therapy for patients with nonspecific CLBP. Meta-regression and subgroup analysis will be also performed to explore the sources of heterogeneity. If there are enough records included, the publish bias will be assessed by funnel plot. All procedures will be strictly performed in accordance with the Cochrane Handbook for Systematic Reviews of Interventions. Conclusion: This review will offer clinical evidence of acupuncture injection therapy for the patients with nonspecific CLBP. PROSPERO Research registration identifying number: CRD42019119158