Dickersonbank4674

Functionally, both SNHG3 silencing and miR-326 overexpression enhanced cell apoptosis, but depressed cell viability, migration and invasion in MDA-MB-231 and BT-549 cells, as well as inhibited Vav2 and Rac1 expression. Selleckchem BIBF 1120 Notably, miR-326 deletion could abolish the tumor-suppressive role of SNHG3 silencing; meanwhile, the similar anti-tumor effect of miR-326 overexpression was abrogated by ITGA5 restoration. Mechanically, SNHG3 silencing downregulated ITGA5 expression by functioning as a molecular "sponge" for miR-326. Conclusions Silencing of SNHG3 suppressed the malignant development of TNBC cells, at least partially, through miR-326/ITGA5 axis and inhibiting Vav2/Rac1 signaling pathway.Objective This study aimed to investigate the expression and role of CT10 regulated kinase like (CRKL) in human laryngeal squamous cell carcinoma (LSCC) progression. Patients and methods Seventy-four laryngeal cancer cases were detected by the immunohistochemistry S-P method and the results were analyzed. RNA interference was used to downregulate the expression of CRKL in Hep-2 cells. The silencing efficiency was detected by real-time PCR and Western blotting. The cell proliferation, migration, and invasion after transfection were detected by MTT, wound healing assay, transwell invasion assay, and apoptosis assay. link2 Western blot was conducted to determine the function of CRKL/epithelial-mesenchymal transition (EMT) signaling pathway. Results The expression of CRKL was higher in LSCC tissues. Patients with higher CRKL expression were correlated with lymph node metastasis and postoperative survival rates. CRKL promoted proliferation, migration, and invasion of Hep-2 cells in vitro. Conclusions These findings suggested that CRKL gene silencing significantly inhibited the proliferation, migration, invasion, and EMT signaling pathway of Hep-2 cells. CRKL is considered to be a new target for the treatment of LSCC.Objective Non-small cell lung cancer (NSCLC) is one of the most ordinary cancers worldwide. Recent studies have discovered many oncogenes play vital roles in the tumorigenesis of malignant tumors. The purpose of our study was to uncover the role of GBP1 in NSCLC and the underlying mechanism. Patients and methods GBP1 expression in NSCLC samples was detected by Real Time quantitative-Polymerase Chain Reaction (RT-qPCR). Function assays were performed in NSCLC cells transfected with GBP1 shRNA. Furthermore, RT-qPCR and Western blot assay were conducted to explore the target signaling pathway of GBP1. Results GBP1 expression was significantly upregulated in NSCLC tissue samples compared with adjacent normal tissues. Function assays showed that the proliferation of NSCLC cells was significantly inhibited via knockdown of GBP1, while cell apoptosis was promoted. Resistance to paclitaxel was reversed after GBP1 knockdown in paclitaxel resistance A549 cells (A549/Taxol). In addition, Wnt/β-catenin signaling pathway was repressed via knockdown of GBP1 in NSCLC cells and A549/Taxol cells. Conclusions In our study, GBP1 was firstly identified as a novel oncogene in NSCLC. Furthermore, it could promote NSCLC development and paclitaxel resistance by inducing Wnt/β-catenin signaling pathway.Objective The study aims to construct a multi-gene risk scoring model that can be used to predict the prognosis of patients with lung squamous cell carcinoma (LUSC). Patients and methods RNA-seq data from 494 LUSC tumor samples and 49 peripheral lung tissue samples were obtained from TCGA_LUSC database. Differential analysis was conducted using edgeR to screen differentially expressed lncRNAs (DElncRNAs) between LUSC and normal samples. Univariate Cox regression analysis was used to screen lncRNAs that were significantly correlated with LUSC prognosis. LASSO regression model was built to reduce complexity. The LUSC prognostic model based on lncRNAs was established by multivariate Cox regression analysis, which was evaluated by ROC curves and survival analysis. ROC and Kaplan-Meier survival curves of each lncRNA in the model were plotted and compared. Results 2085 DElncRNAs were identified. Combined with univariate Cox regression analysis, 342 prognosis-related genes were screened. After LASSO regression analysis, 11 lncRNAs tightly related to LUSC prognosis were identified and a risk scoring model was constructed. ROC curve analysis proved the good performance of the model. The Kaplan-Meier survival curve showed that the mortality in high-risk group was significantly higher. The survival analysis results of each lncRNA were also consistent with the prediction in Cox regression. Conclusions Our results suggested that the 11-lncRNA risk scoring model may provide a new insight for predicting prognosis of LUSC patients.Objective Non-small cell lung cancer (NSCLC) accounts for the majority of lung cancer, with an unfavorable prognosis of 5-year survival rates. It is of great clinical significance to further search for more efficacious and novel targets for diagnosis and therapeutic strategies. This study aimed at clarifying the role of long non-coding RNA (lncRNA) NORAD in proliferation, invasion and migration and tumor growth of NSCLC. Materials and methods In this study, mRNA levels of lncRNA NORAD were examined by RT-PCR. CCK-8 assay was applied to test cell viability. Furthermore, wound healing assay and transwell assay were performed to detect the migration and invasion of A549 cells, respectively. Immunohistochemistry was applied to assess the levels of CXC chemokine receptor (CXCR) 4 and CXC chemokine ligand (CXCL) 12. Mice models of NSCLC in vivo were exploited to further examine the potential role of NORAD in tumor growth. Key proteins related to Ras homolog gene family member A (RhoA) GTPase/Rho-associated kinase (RhoA/ROCK) pathway were determined by Western blot. Results NORAD has elevated the levels in NSCLC tissues and cells. NORAD interference dramatically inhibited tumor growth and suppressed A549 cell proliferation, migration and invasion by downregulating CXCR4 and CXCL12 expression. RhoA/ROCK signaling pathway was activated in NSCLC. link3 Conclusions This study revealed that the downregulation of lncRNA NORAD could slow down the progression of NSCLC by regulating CXCR4 and RhoA/ROCK signaling pathway.Objective CSE1L (human chromosomal segregation 1-like) is reported to be able to affect cell apoptosis, invasiveness, and migration. The purpose of this study was to uncover the regulatory effects of CSE1L on cell phenotypes of oral cancer and the underlying mechanism. Materials and methods CSE1L levels in oral cancer cells were determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) and Western blot. CSE1L overexpression and knockdown models were constructed in CAL-27 and HN6 cells, respectively. Changes in proliferative and migratory abilities in oral cancer cells affected by CSE1L and microphthalmia-associated transcription factor (MITF) were assessed by cell counting kit-8 (CCK-8), 5-Ethynyl-2'-deoxyuridine (EdU) and wound healing assay. Meanwhile, potential influences of CSE1L and MITF on relative levels of E-cadherin and Vimentin in oral cancer cells were detected. Finally, regulatory effects of CSE1L and MITF on the Akt/mTOR pathway were evaluated by detecting expression levels of p-Akt, Akt, p-mTOR, and mTOR. Results CSE1L was upregulated in oral cancer cells. Knockdown of CSE1L in HN6 cells attenuated proliferative and migratory abilities, as well as downregulated Vimentin and upregulated E-cadherin. Overexpression of CSE1L in CAL-27 cells yielded the opposite results. MIFT level was positively regulated by CSE1L. Overexpression of MITF partially reversed regulatory effects of CSE1L on proliferative ability of oral cancer cells. Moreover, silence of CSE1L suppressed the Akt/mTOR pathway, which was reversed by overexpression of MITF. Conclusions CSE1L promotes the proliferative and migratory abilities in oral cancer cells by positively regulating MITF, thus activating the Akt/mTOR pathway.Objective This study was designed to investigate the expression characteristics of CSN6 in oral squamous cell carcinoma (OSCC), and to further explore the mechanism of how it promotes the malignant progression of this cancer. Patients and methods The expressions of CSN6 and TIMP-2 in tumor tissue samples and adjacent normal ones collected from 36 OSCC patients were detected via quantitative Real Time-Polymerase Chain Reaction (qRT-PCR), and the interplay between their expression levels and the clinical indicators or prognosis of OSCC patients was analyzed as well. Meanwhile, the expressions of CSN6 and TIMP-2 in OSCC cell lines were further verified via qRT-PCR. In addition, CSN6 overexpression and knockdown models were constructed using lentivirus in OSCC cell lines, CAL-27, and Tca8113. At the same time, transwell and cell wound healing assays were conducted to uncover the impact of CSN6 on the function of OSCC cells. Finally, the potential mechanism was explored using Luciferase reporter gene and recovery t CSN6 was remarkably upregulated both in OSCC tissues and cell lines, which is remarkably relevant to the incidence of lymph node or distant metastasis and poor prognosis of OSCC patients. Additionally, we verified that CSN6 may promote OSCC malignant progression by regulating TIMP-2.Objective Identification of novel and reliable biomarkers is crucial for the early detection and prognosis prediction of esophageal squamous cell carcinoma (ESCC). In this study, we aimed to explore the potential clinical significance of serum exosomal miR-182 in ESCC. Patients and methods A total of 125 patients with ESCC and 60 healthy volunteers were enrolled in this study. Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was used to detect the serum exosomal miR-182 level. Then, the associations between serum exosomal miR-182 levels and clinicopathological features, as well as clinical outcome were further investigated. Results Serum exosomal miR-182 levels were significantly higher in pre-operative ESCC patients than in normal controls and post-operative ESCC patients. In addition, the receiver operating characteristic (ROC) curve analysis showed that the serum exosomal miR-182 could well differentiate ESCC patients from the healthy controls. Moreover, high serum exosomal miR-182 expression was strongly associated with worse clinical parameters including differentiation, lymph node metastasis, and TNM stage. ESCC patients in the high serum exosomal miR-182 group had significantly shorter overall survival and relapse free survival than those in the low serum exosomal miR-182 group. Furthermore, serum exosomal miR-182 was an independent prognostic indicator for ESCC. Conclusions Collectively, serum exosomal miR-182 might serve as a promising biomarker for predicting the unfavorable prognosis of ESCC.Objective The aim of this study was to investigate the expression of long non-coding ribonucleic acid (lncRNA) AK058003 in esophageal carcinoma (EC) tissues, and to analyze its intervention effect. Patients and methods The expression of lncRNA AK058003 in EC tissues and para-carcinoma tissues from 130 EC patients was detected via quantitative Polymerase Chain Reaction (qPCR). EC cell lines were selected for exogenous interference in lncRNA AK058003. Subsequently, the expression of lncRNA AK058003 in normal esophageal epithelial cell line (Het-1A) and EC cell lines (EC109, EC9706, KYSE-150, KYSE-30, and TE-1) was detected by qPCR. EC9706 cell lines with the highest expression of lncRNA AK058003 were selected and transfected with lncRNA AK058003 siRNA and lncRNA AK058003 control, respectively. After transfection, the expression of lncRNA AK058003 was determined using PCR. The changes in cell growth and proliferation were analyzed via cell growth curve and cell cycle assay. Meanwhile, the changes in cell migration and invasion were analyzed through wound healing assay.