gene expression was notably increased in the disease group. There was an association between GG genotype at c-myc gene locus rs121918684 and LDH level (p=0.000), between CT genotype at c-myc gene locus rs775522201 and PLT level (p=0.002), and between AA genotype at K-ras gene locus rs1137188 and Hb level (p=0.003). CONCLUSIONS The c-myc and K-ras gene polymorphisms are associated with susceptibility to NHL, gene expression and levels of Hb, PLT, and LDH.OBJECTIVE The aim of this study was to explore the expression of long non-coding RNA (lncRNA) MIR31HG in malignant melanoma (MM), and to investigate its clinical significance. PATIENTS AND METHODS The quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was used to detect the expression of lncRNA MIR31HG in MM tissues and cells. The relationship between lncRNA MIR31HG expression and the clinicopathological characteristics was analyzed. Furthermore, the cell counting kit-8 (CCK-8) and the transwell assays were performed to assess the effect of MIR31HG on cell proliferation and metastasis in vitro, respectively. RESULTS The expression of MIR31HG was significantly upregulated in MM tissues and cells. selleckchem To explore the relationship between MIR31HG expression and clinical features, the patients were divided into two groups according to the mean expression of MIR31HG, including high expression group and low expression group. The subsequent results indicated that MIR31HG expression was correlated with lymph nodes metastasis, distal metastasis, and TNM stage. The multivariate analysis indicated that a high expression of MIR31HG could be used as an independent prognostic factor for MM. MIR31HG low-expression cells were constructed in vitro. Compared with the control cells, the cells with low expression of MIR31HG showed significantly low malignancy, including decreased cell proliferation rate and migration and invasion rates. CONCLUSIONS LncRNA MIR31HG was a novel factor involved in MM progression, which could be used as a potential biomarker and therapeutic target for MM.OBJECTIVE The aim of this study was to elucidate whether FOXD2-AS1 stimulated glioma progression by inhibiting the P53 level. PATIENTS AND METHODS FOXD2-AS1 expression in glioma tissues and cell lines was determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Meanwhile, FOXD2-AS1 expression in glioma patients with different tumor tissues and tumor staging was examined as well. The subcellular distribution of FOXD2-AS1 was analyzed. RNA Binding Protein Immunoprecipitation (RIP) and Chromatin immunoprecipitation (ChIP) assay were applied to explore the interaction between FOXD2-AS1 and P53. Furthermore, the influences of FOXD2-AS1 and P53 on the viability and colony formation abilities of LN229 and U87 cells were assessed. RESULTS FOXD2-AS1 was significantly upregulated in glioma tissues and cells. The expression level of FOXD2-AS1 was positively correlated with tumor size and staging of glioma. FOXD2-AS1 was mainly distributed in the nucleus, which could attenuate recruitment ability to P53 by bounding to EZH2. The silence of FOXD2-AS1 significantly decreased the viability and colony formation abilities of glioma cells. However, the attenuated proliferative ability was partially reversed by P53 knockdown. CONCLUSIONS FOXD2-AS1 stimulated the proliferation of glioma by inhibiting P53, thus aggravating the progression of glioma.OBJECTIVE To discuss the role and mechanism of β4GalT1 both in vivo and in vitro glioma, observe whether pathophysiological processes of glioma can be improved after β4GalT1 is knocked down, and study whether β4GalT1 plays a role in malignant biological processes of glioma by regulating the apoptosis and immune processes. PATIENTS AND METHODS Firstly, the distribution difference of β4GalT1 in tumor tissues and normal tissues was analyzed by Gene Expression Profiling Interactive Analysis (GEPIA) tumor analysis system to deduce the possible role of β4GalT1 in glioma. Secondly, whether the malignant degree of glioma was related to the expression of β4GalT1 and its immunity using human tumor tissues and blood lymphocyte subsets was analyzed. Thirdly, interfere lentivirus vector with β4GalT1 and knockdown β4GalT1 was analyzed to observe whether the malignant degree of glioma has changed. Fourthly, interfere lentivirus vector with recombinant β4GalT protein and β4GalT1 was analyzed to verify the effect of β4GalT in1 is knocked down. During the development of glioma, β4GalT1 may play a malignant biological role through inflammatory response.OBJECTIVE The aim of this study was to explore the expression of long non-coding ribonucleic acid (lncRNA) FALEC (hereinafter referred to as FALEC) in papillary thyroid carcinoma (PTC) and its effects on the proliferation, invasion, and metastasis of PTC cells. PATIENTS AND METHODS Quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR) was performed to measure the expression level of FALEC in 48 cases of PTC tissues and cells. The small interfering (si)-FALEC was synthesized and transfected into PTC cells. Interference efficiency was confirmed via qRT-PCR assay. Subsequently, the effect of FALEC on the proliferation of PTC cells was determined by cell counting kit-8 (CCK-8) assay. Wound healing and transwell assays were conducted to detect the effects of FALEC on the invasion, migration, and metastasis of PTC cells. Additionally, changes in the protein expression of Wnt/β-catenin signaling pathway molecular markers was detected via Western blotting. RESULTS The expression level of FALEC was significantly higher in PTC tissues than that of adjacent normal tissues. FALEC expression was significantly up-regulated in PTC cell lines, as well. CCK-8 assay revealed that the proliferation ability of PTC cells was remarkably weakened after down-regulation of FALEC in vitro. Wound healing and transwell assays demonstrated that, compared with si-normal control (NC) group, the migration and invasion capabilities declined significantly in si-FALEC group. Furthermore, the Western blotting analysis indicated that the expression of Wnt/β-catenin signaling pathway molecular markers was changed after the interference in FALEC expression. CONCLUSIONS FALEC expression was up-regulated in PTC tissues and cell lines. Highly expressed FALEC facilitated the proliferation, migration, and invasion of PTC by regulating the Wnt/β-catenin signaling pathway.