This study was to explore the role of ELOVL6 in the development of head and neck squamous cell carcinoma (HNSCC). Considering its previously identified oncogenic role in hepatocellular carcinoma. ELOVL6 gene expression, clinicopathological analysis, enrichment analysis, and immune infiltration analysis were based on the data from Gene Expression Omnibus and The Cancer Genome Atlas, with additional bioinformatics analyses performed. Human HNSCC tissue microarray and cell lines were used. The expression of ELOVL6 in HNSCC was detected by quantitative polymerase chain reaction, immunohistochemistry assay, and western blot analysis. The proliferation ability of HNSCC cells, invasion, and apoptosis were evaluated using cell counting kit-8 method, Transwell assay, and flow cytometry, respectively. Based on the data derived from the cancer databases and our HNSCC cell and tissue studies, we found that ELOVL6 was overexpressed in HNSCC. Moreover, ELOVL6 expression level had a positive correlation with clinicopathology of HNSCC. Gene set enrichment analysis showed that ELOVL6 affected the occurrence of HNSCC through WNT signaling pathway. Functional experiments demonstrated that ELOVL6 knockdown inhibited the proliferation and invasion of HNSCC cells while promoting apoptosis. Additionally, compound 3f, an agonist of WNT/β-catenin signaling pathway, enhances the effect of ELOVL6 on the progression of HNSCC cells. ELOVL6 is upregulated in HNSCC and promotes the development of HNSCC cells by inducing WNT/β-catenin signaling pathway. ELOVL6 stands a potential target for the treatment of HNSCC and a prognosis indicator of human HNSCC.

MicroRNAs(miRNAs) are maladjusted in multifarious malignant tumor and can be considered as both carcinogens and tumor-inhibiting factor. In the present study, we analyzed the miRNAs expression profiles and clinical information of 481 patients with head and neck squamous cell carcinoma (HNSCC) through the TCGA dataset to identify the prognostic miRNAs signature. A total of 114 significantly differentially expressed miRNAs (SDEMs) were identified, consisting of 60 up-adjusted and 54 down-adjusted miRNAs. The Kaplan-Meier survival method identified the prognostic function of 2 miRNAs (miR-4652-5p and miR-99a-3P). Univariate and multivariate Cox regression analyses indicated that the 2 miRNAs were significant prognostic elements of HNSCC. Furthermore, bioinformatic analysis was conducted by means of 4 online gene predicted toolkits to recognize the target genes, and enrichment analysis was performed on the target genes by DAVID. The outcomes depicted that target genes were correlated with calcium, as well as cell proliferation, circadian entrainment, EGFR, PI3K-Akt-mTOR, and P53 signaling pathways. Finally, the PPI network was conducted in view of STRING database and Cytoscape. Eight hub genes were identified by CytoHubba and MCODE app, respectively, CBL, SKP1, H2AFX, HGF, POLR2F, UBE2I, VAMP2, and GNAI2 genes. As a result, we identified 2 miRNAs signatures, 8 hub genes, and significant signaling pathways for estimating the prognosis of HNSCC. In order to further explore the molecular mechanism of HNSCC occurrence and development, more comprehensive basic and clinical studies are needed.

The insulin-like growth factor binding protein 6 (IGFBP6), as an inhibitor of IGF-II actions, plays an important role in inhibiting survival and migration of tumor cells. In our study, we intended to demonstrate the biological function of IGFBP6 in the development of glioma and its clinical significance. Firstly, Western blot and immunohistochemistry revealed that the expression of IGFBP6 inversely correlated with glioma grade. Secondly, multivariate analysis with the Cox proportional hazards model and Kaplan–Meier analysis indicated that IGFBP6 could be an independent prognostic factor for the survival of glioma patients. In addition, overexpression of IGFBP6 induced glioma cell apoptosis, and depletion of IGFBP6 had the opposite action. Finally, overexpression of IGFBP6 inhibited migration of glioma cells, and depletion of IGFBP6 had the opposite action. Together our findings suggest that IGFBP6 might be an important regulator and prognostic factor for glioma.

Glioma is one of the most common and aggressive types of human brain tumor, it is important to explore novel glioma-associated genes. In this report, we defined Gpx4 as a therapeutic target for glioma. Western blot and immunohistochemistry(IHC) analysis revealed that the protein level of Gpx4 was higher in glioma tissues and cell lines. In addition, IHC stain revealed that there was statistical significance between the expression of Gpx4 and the WHO grade (P=0.004) and Ki-67(P=0.000) expression. Kaplan-Meier curve showed that high expression of Gpx4 was associated with poor prognosis of glioma patients (P<0.01). To determine whether Gpx4 could regulate the proliferation and migration of glioma cells, we transfected glioma cells with Gpx4-siRNA and then investigated cell proliferation with cell counting kit (CCK) -8, flow cytometry assay and colony formation analyses, and we used wound-healing and transwell assays to investigate cell migration. Our results indicated that knockdown of Gpx4 would inhibit the proliferation and migration of glioma cells. Besides, silencing of Gpx4 could induce the apoptosis of glioma cells. This research indicated that Gpx4 might be thought of as a new prognostic factor in glioma and be closely correlated with glioma cell proliferation, migration and apoptosis.

Background: To investigate the mechanisms underlying the regulation of human glioma cell growth, proliferation, and apoptosis by microRNA-17 (miR-17) to provide targets for novel human glioma therapies.Methods: The expression of miR-17 in human glioma tissues and cell lines was detected using real-time quantitative PCR (qRT-PCR). A miR-17 inhibitor was transfected into the U251 human glioma cell line using liposomes, and changes in miR-17 expression were detected using qRT-PCR. The effects of miR-17 on numerous biological characteristics of U251 cells, including viability, proliferation, apoptosis, and migration, were analyzed using MTT, flow cytometry, and Transwell migration chamber assays. A luciferase reporter gene system was used to validate SAM- and SH3-domain containing 1 (SASH1) as a true target of miR-17. The effects of miR-17 on SASH1 protein expression were determined using western blotting.Results: qRT-PCR results showed that compared with adjacent tissues, miR-17 expression was significantly increased in human glioma tissues and cells lines (P<0.001). Compared with the control group, miR-17 expression in the miR-17 inhibitor transfection group was significantly decreased (P<0.01). The results of the MTT, flow cytometry, and Transwell migration chamber assays showed that cell viability (P<0.05), G2M+S phase fraction (P<0.05), and migration ability (P<0.05) in the miR-17 inhibitor transfection group was significantly decreased compared with the normal control and inhibitor control groups. Flow cytometry showed that apoptosis in the miR-17 inhibitor transfection group was increased compared with the normal control and inhibitor control groups (P<0.05). Relative luciferase activity in the miR-17 mimic group was significantly decreased compared with the control group (P<0.05). Western blotting revealed that SASH1 protein expression in the miR-17 inhibitor transfection group was significantly increased compared with the normal control and inhibitor control groups (P<0.05).Conclusions: miR-17 promotes viability, proliferation, and migration and inhibits apoptosis in U251 glioma cells, and these mechanisms could be mediated by the regulation of SASH1 gene expression.

The association between whole and refined grain consumption and stroke risk remains unclear. A search using MEDLINE and EMBASE databases was performed through February 29, 2016. Seven prospective studies with a total of 446 451 subjects and 5892 stroke events were included. The summary relative risk (SRR) of stroke for the high versus low consumption was 0.95 (95% confidence interval [CI] = 0.83-1.14) for total grains, 0.92 (95% CI = 0.72-1.17) for whole grains, and 0.99 (95% CI = 0.84-1.16) for refined grains. Diets rich in whole grains were inversely associated with ischemic stroke risk (SRR = 0.75, 95% CI = 0.60-0.95). Our meta-analysis revealed that whole and refined grain consumption is not associated with total stroke risk; however, whole grain consumption is associated with reduced ischemic stroke risk.

B23 (also known as Nucleophosmin, NPM, numatrin or NO38) is a ubiquitously expressed phosphoprotein belonging to the nucleoplasmin family of chaperones. In this study we intended to investigate the clinical significance of B23 expression in human glioma and its biological function in glioma cells. Western blot and immunohistochemistry analysis showed that B23 was overexpressed in glioma tissues and glioma cell lines. In addition, the expression level of B23 was positively correlated with glioma pathological grade and Ki-67 expression. Kaplan-Meier analysis revealed that a higher B23 expression in patients with glioma was associated with a poorer prognosis. In vitro, after the release of glioma cell lines from serum starvation, the expression of B23 was upregulated, as well as PCNA (Proliferating Cell Nuclear Antigen) and cyclin A. In addition, knockdown of B23 by small interfering RNA transfection diminished the expression of PCNA, cyclin D1 and arrested cell growth at G1 phase. Taken together, our results implied that B23 could be a candidate prognostic biomarker as well as a potential therapeutical target of glioma.

The purpose of this study was to investigate the impact of SAM- and SH3-domain containing 1 (SASH1) on the biological behavior of glioma cells, including its effects on cellular growth, proliferation, apoptosis, invasion, and metastasis, and thereby to provide an experimental basis for future therapeutic treatments. A pcDNA3.1-SASH1 eukaryotic expression vector was constructed and transfected into the U251 human glioma cell line. Using the tetrazolium-based colorimetric (MTT) assay, flow cytometry analyses, transwell invasion chamber experiments, and other methods, we examined the impact of SASH1 on the biological behaviors of U251 cells, including effects on viability, cell cycle, apoptosis, and invasion. Furthermore, the effect of SASH1 on the expression of cyclin D1, caspase-3, matrix metalloproteinase (MMP)-2, MMP-9, and other proteins was observed. Compared to the empty vector and blank control groups, the pcDNA3.1-SASH1 group of U251 cells exhibited significantly reduced cell viability, proliferation, and invasion ( p < 0.05), although there was no difference between the empty vector and blank control groups. The pcDNA3.1-SASH1 group demonstrated a significantly higher apoptotic index than did the empty vector and blank control groups ( p < 0.05), and the percentage of apoptotic cells was similar between the empty vector and blank control groups. In addition, the pcDNA3.1-SASH1 group expressed significantly lower protein levels of cyclin D1 and MMP-2/9 compared to the control and empty vector groups ( p < 0.05) and significantly higher protein levels of caspase-3 than the other two groups ( p < 0.05). Cyclin D1, caspase-3, and MMP-2/9 expression was unchanged between the empty vector and blank control groups. SASH1 gene expression might be related to the inhibition of the growth, proliferation, and invasion of U251 cells and the promotion of U251 cells apoptosis.