Pearcemagnussen0087

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. 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.OBJECTIVE Recent studies have corroborated that circular RNAs (circRNAs) as endogenous noncoding RNAs gain research interest in carcinogenesis, functioning as prognostic and diagnostic biomarkers and therapeutic targets. The present study is aimed to determine whether circRNAs could serve as prognostic and diagnostic biomarkers to predict thyroid carcinoma. MATERIALS AND METHODS High-throughput sequencing analysis was conducted to detect circRNAs expression profile in thyroid cancer. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) measurement was utilized to validate circRNAs expression in blood and tissue specimens. Kaplan-Meier method and receiver operating characteristic (ROC) curves and the area under the ROC curve (AUC) were used to assess whether circRNAs could function as prognostic and diagnostic biomarkers of thyroid cancer, respectively. RESULTS Hsa_circ_0124055 and hsa_circ_0101622 as the most conspicuous biomarkers were significantly increased in tumor tissues and plasma of thyroid cancer patients. High hsa_circ_0124055 or hsa_circ_0101622 expression exhibited shorter overall survival. Our findings also provided strong evidence that plasma hsa_circ_0124055 (AUC = 0.836, 95% CI 0.763-0.908, p less then 0.001) and hsa_circ_0101622 (AUC = 0.805, 95% CI 0.727-0.883, p less then 0.001) could be used as diagnostic markers for thyroid cancer, and hsa_circ_0124055 combined with hsa_circ_0101622 could provide a more powerful diagnostic value (AUC = 0.911, 95% CI 0.859-0.962, p less then 0.001) than the use of hsa_circ_0124055 or hsa_circ_0101622 alone. Furthermore, the knockdown of hsa_circ_0124055 or hsa_circ_0101622 exhibited a significant anti-proliferative and pro-apoptotic activity of thyroid cancer cells in vivo and in vitro. CONCLUSIONS Both hsa_circ_0124055 and hsa_circ_0101622 could facilitate the prognosis and diagnosis of thyroid cancer, and function as the therapeutic targets for clinical practice.OBJECTIVE This research was designed to explore the expression characteristics of microRNA-9501 in breast cancer (BCa), and to further explore whether it can influence the development of BCa through the regulation of Wnt/β-Catenin pathway. PATIENTS AND METHODS QPCR was carried out to examine microRNA-9501 level in tumor tissue samples and paracancerous ones collected from 42 BCa patients, and the interplay between microRNA-9501 expression and the clinical indicators, as well as the prognosis of BCa patients were analyzed. In addition, we detected microRNA-9501 expression in BCa cell lines by qPCR. Subsequently, microRNA-9501 overexpression model was constructed in BCa cell lines MCF-7 and MDA-MB-231. Then, CCK-8, EdU, cell wound healing, as well as transwell assays, were carried out to evaluate the impact of microRNA-9501 on the biological functions of BCa cells. Finally, the Dual-Luciferase reporting test and tumor formation experiment in nude mice were conducted to further clarify the potential molecular mehat microRNA-9501 may suppress the malignant growth of breast tumor. CONCLUSIONS MicroRNA-9501 expression was found remarkably decreased in BCa tissues and cell lines, which was closely relevant to the pathological stage, metastasis incidence, and prognosis of BCa patients. In addition, microRNA-9501 may suppress the malignant progression of BCa via modulating Wnt/β-Catenin path-way.OBJECTIVE The aim of this study was to investigate whether METTL3 promoted the progression of nasopharyngeal carcinoma (NPC) by silencing CDKN1C through EZH2. PATIENTS AND METHODS Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was performed to examine the expression level of METTL3 in 48 pairs of NPC tissues and adjacent normal tissues. METTL3 expression in patients with different tumor lymph node metastasis (TNM) stages was detected by qRT-PCR as well. The Kaplan-Meier method was used to analyze the interplay between METTL3 expression and the prognosis of patients with NPC. At the same time, METTL3 expression in normal epithelial cell line (BEAS-2B) and NPC cell lines (SUNE-1 and C666-1) was examined using qRT-PCR. After METTL3 was knocked down in SUNE-1 cells, cell viability and migration abilities were analyzed by cell counting kit-8 (CCK-8) test and wound healing assay, respectively. The mRNA and protein expressions of EZH2 were detected by qRT-PCR and Western blot, respectively. RNA immunopre CONCLUSIONS METTL3 was highly expressed in NPC tissues, which might inhibit EZH2 expression by mediating M6A modification of EZH2 mRNA. Furthermore, CDKN1C could increase the malignancy of NPC cells and promote the progression of NPC.OBJECTIVE As a kind of non-coding RNA, circular RNA (circRNA) plays a regulatory role in many tumors. Our intention was to investigate the clinical significance, biological function, and molecular regulation mechanisms of circ_0067934 in laryngeal squamous cell cancer (LSCC) progression. PATIENTS AND METHODS The expression levels of circ_0067934 in LSCC tumor samples and cells were determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The associations of circ_0067934 expression with clinicopathological features and overall survival in LSCC patients were statistically analyzed. The biological function of circ_0067934 in LSCC cells was analyzed by CCK-8, colony formation, EdU, and transwell assays. Dual-Luciferase reporter assay was conducted to verify that circ_0067934 may sponge miR-1324 to regulate proliferation and migration of LSCC. RESULTS Circ_0067934 expression was remarkably upregulated in LSCC tissues and cells. High level of circ_0067934 was significantly related to tumor size, lymph node status, and distant metastasis of LSCC.