SNORA71A Promotes Colorectal Cancer Cell Proliferation, Migration, and Invasion.

Small nucleolar RNAs (snoRNAs) play a crucial role during colorectal cancer (CRC) development. The study of SNORA71A is few, and its role in CRC is unknown. This study focused on screening abnormal snoRNAs in CRC and exploring the role of key snoRNA in CRC.

Long Noncoding RNAs Serve as Potential Diagnostic Biomarkers for Colorectal Cancer.

Mounting evidence has indicated that long noncoding RNAs (lncRNAs) are promising candidates for tumor diagnosis and prognosis. Nonetheless, the significance of lncRNAs in colorectal cancer (CRC) diagnosis remains to be clarified. Here, we performed a comprehensive meta-analysis to evaluate the utility of lncRNAs as diagnostic indicators for CRC.

Prognostic value and clinical significance of long noncoding RNA CASC2 in human malignancies: a meta-analysis.

Purpose: This meta-analysis aimed to assess the prognostic value of long noncoding RNA cancer susceptibility candidate 2 (CASC2) in human tumors.

Materials And Methods: We searched the available databases up to December 2017. Pooled hazard ratios (HRs) and the corresponding 95% confidence intervals (CIs) were used to examine the prognostic impact of CASC2 on overall survival (OS) in patients diagnosed with malignancies.

Selective inhibition of endothelial NF-κB signaling attenuates chronic intermittent hypoxia-induced atherosclerosis in mice.

Background And Aims: Chronic intermittent hypoxia (CIH) exposure causes atherosclerosis, although the underlying mechanisms are poorly understood. This study defines the role of endothelial intrinsic NF-κB signaling in the atherogenic response to CIH.

Methods: We created ApoE-EC mice that are deficient in the apolipoprotein E gene (ApoE) and overexpress an I-κBα mutant (I-κBmt) selectively in endothelial cells.

CD146 Promoter Polymorphism (rs3923594) Is Associated with Recurrence of Clear Cell Renal Cell Carcinoma in Chinese Population.

Introduction: CD146 is a membrane signal receptor in tumor-induced angiogenesis. However, limited studies have focused on the CD146 promoter polymorphisms in clear cell renal cell carcinoma (ccRCC).

Purpose: The purpose of this study was to investigate the association between polymorphisms located in the promoter region of the CD146 gene and characteristics of ccRCC in Chinese population.

Diabetes and the risk of biochemical recurrence in patients with treated localized prostate cancer: a meta-analysis.

Background: Biochemical recurrence (BCR), or an elevation in prostate-specific antigen in men after treatment for localized prostate cancer, is an early indication of clinical progression, distant metastases, and mortality. Correlations have also recently been established between diabetes and the incidence and mortality of prostate cancer. However, it remains unknown whether diabetes may predict BCR.

Relationship between toxicities and clinical benefits of newly approved tyrosine kinase inhibitors in thyroid cancer: A meta-analysis of literature.

Background: The aim of this meta-analysis was to analyze the relationship of toxicities and clinical benefits of newly approved lenvatinib and sorafenib to thyroid cancer (TC) in patients.

Materials And Methods: Three major medical databases, PubMed, EMBASE, and ISI web of science were systematically searched to identify all studies on lenvatinib and sorafenib in TC. A meta-analysis was performed to clarify the toxicities and clinical benefits of newly Food and Drug Administration (FDA) approved lenvatinib and sorafenib to thyroid cancer.

RNAi-mediated RPL34 knockdown suppresses the growth of human gastric cancer cells.

An increasing body of evidence suggests that ribosomal proteins may have ribosome-independent functions and may be involved in various physiological and pathological processes. To examine the role of ribosomal protein L34 (RPL34) in cancer transformation, we assessed its expression in gastric cancer cell lines and found it highly expressed. We further used lentivirus-mediated small interfering RNAs (siRNAs) to knockdown RPL34 expression in the human gastric cancer cell line SGC-7901.

LPS Down-Regulates Specificity Protein 1 Activity by Activating NF-κB Pathway in Endotoxemic Mice.

Background: Specificity protein (Sp) 1 mediates the transcription of a large number of constitutive genes encoding physiological mediators. NF-κB mediates the expression of hundreds of inducible genes encoding pathological mediators. Crosstalk between Sp1 and NF-κB pathways could be pathophysiologically significant, but has not been studied.

Resident Endothelial Cells and Endothelial Progenitor Cells Restore Endothelial Barrier Function After Inflammatory Lung Injury.

Objective: Disruption of endothelial barrier integrity is a characteristic of many inflammatory conditions. However, the origin and function of endothelial cells (ECs) restoring endothelial barrier function remain unknown. This study defined the roles of resident ECs (RECs) and bone marrow-derived endothelial progenitor cells (BMDEPCs) in endothelial barrier restoration after endotoxemic lung injury.

Methylation of DLEC1 promoter is a predictor for recurrence in Chinese patients with gastric cancer.

Purpose: To investigate promoter methylation in the deleted in lung and esophageal cancer 1 (DLEC1) gene in Chinese patients with gastric cancer.

Methods: A total of 227 patients with gastric cancer were enrolled. The methylations of the promoter regions of DLEC1 and ACTB were determined using quantitative methylation-specific PCR.

Association of CA 15-3 and CEA with clinicopathological parameters in patients with metastatic breast cancer.

The objective of this study was to investigate the association of serum cancer antigen 15-3 (CA 15-3) and carcinoembryonic antigen (CEA) levels with clinicopathological parameters in patients diagnosed with metastatic breast cancer (MBC). We retrospectively evaluated the medical records of 284 patients diagnosed with MBC between January, 2007 and December, 2012 who fulfilled the specified criteria and the association between the levels of the two tumor marker and clinicopathological parameters was analyzed. Of the 284 patients, elevated CA 15-3 and CEA levels at initial diagnosis of recurrence were identified in 163 (57.

An obligatory role of NF-κB in mediating bone marrow derived endothelial progenitor cell recruitment and proliferation following endotoxemic multiple organ injury in mice.

Background: Recruitment of bone marrow derived endothelial progenitor cells (BMDEPCs) alleviates multiple organ injury (MOI) and improves outcomes. However, mechanisms mediating BMDEPC recruitment following septic MOI remain largely unknown. This study characterized the kinetics of BMDEPC recruitment and proliferation and defined the role of NF-κB in regulating BMDEPC recruitment and proliferation.

NF-κB-to-AP-1 switch: a mechanism regulating transition from endothelial barrier injury to repair in endotoxemic mice.

Endothelial barrier disruption is a hallmark of multiple organ injury (MOI). However, mechanisms governing the restoration of endothelial barrier function are poorly understood. Here, we uncovered an NF-κB-to-AP-1 switch that regulates the transition from barrier injury to repair following endotoxemic MOI.

Prognostic prediction and diagnostic role of intercellular adhesion molecule-1 (ICAM1) expression in clear cell renal cell carcinoma.

The intercellular adhesion molecule-1 (ICAM1) has been reported to function in multiple malignancies, but its effect on clear cell renal cell carcinoma (ccRCC) hasn't been discussed yet. This study aimed to identify the potential role of ICAM1 in prognostic prediction and early diagnosis of ccRCC. ICAM1 expression was inspected by immunohistochemistry and correlated with clinicopathologic variables.

Quantification of plasma cell-free DNA in predicting therapeutic efficacy of sorafenib on metastatic clear cell renal cell carcinoma.

Purpose: The objective of this study is to determine whether or not plasma cfDNA levels can predict efficacy of sorafenib in patient with metastatic cRCC.

Materials And Methods: Plasma cfDNA levels were quantified by quantitative real-time PCR at six different time-points (before treatment, 4 weeks, 8 weeks, 12 weeks, 16 weeks, and 24 weeks) in 18 metastatic cRCC patients receiving sorafenib, as assessed by CT examination according to RECIST 1.1.

Association of nesfatin-1 and fat mass in cystic fibrosis.

Background: The mechanisms of fat mass (FM) loss in cystic fibrosis (CF) are poorly understood but could represent complex pathways involving dysregulation of appetite-modulating peptides and an amplified inflammatory response. Nesfatin-1 is a newly described peptide that decreases food intake and FM but has not been studied in CF.

Objectives: We hypothesized that changes in the appetite-suppressing hormone nesfatin-1 would be physiological, and levels would be lower in advanced CF patients with lower FM compared to those with milder disease and healthy controls.

Chronic intermittent hypoxia down-regulates endothelial nitric oxide synthase expression by an NF-κB-dependent mechanism.

Objectives: Patients with obstructive sleep apnea have an impaired endothelium-dependent vasodilator response. The mechanisms underlying this impairment remain unclear. We tested the hypothesis that chronic intermittent hypoxia (CIH) impairs endothelium-dependent vasodilatation by NF-κB-mediated down-regulation of endothelial nitric oxide synthase (eNOS) expression.

Chronic intermittent hypoxia exposure induces atherosclerosis in ApoE knockout mice: role of NF-κB p50.

Current animal models of chronic intermittent hypoxia (CIH)-induced atherosclerosis have limitations. Mechanisms of CIH-induced atherosclerosis are poorly understood. This study tested new mouse models of CIH-induced atherosclerosis and defined the role of NF-κB p50 in CIH-induced atherosclerosis.

Epigenetic inactivation of deleted in lung and esophageal cancer 1 gene by promoter methylation in gastric and colorectal adenocarcinoma.

Background/aim: Deleted in Lung and Esophageal Cancer 1 (DLEC1) gene was a new candidate tumor suppressor gene, we evaluated the diagnostic role of DLEC1 methylation in gastric adenocarcinoma (GAC) and colorectal adenocarcinoma (CRAC).

Methodology: Methylation-specific polymerase chain reaction (MSP) was used to determine the promoter methylation status of DLEC1 gene in tissue and serum DNA. DLEC1 gene expression was determined by immunohistochemistry.

Selective blockade of endothelial NF-kappaB pathway differentially affects systemic inflammation and multiple organ dysfunction and injury in septic mice.

Endothelium has long been considered both a source and a target of systemic inflammation. However, to what extent endothelial activation contributes to systemic inflammation remains unclear. This study addresses the relative contribution of endothelial activation to systemic inflammation and multiple organ dysfunction and injury (MOD/I) in an E.

A pivotal role of endothelial-specific NF-kappaB signaling in the pathogenesis of septic shock and septic vascular dysfunction.

Although the role of NF-kappaB in the pathogenesis of sepsis and septic shock has been extensively studied, little is known about the causative contribution of endothelial-intrinsic NF-kappaB to these pathological processes. In this study, we used transgenic (TG) mice (on FVB genetic background) that conditionally overexpress the NF-kappaB inhibitor, mutant I-kappaBalpha, selectively on endothelium and their transgene-negative littermates (wild type (WT)) to define the causative role of endothelial-specific NF-kappaB signaling in septic shock and septic vascular dysfunction. In WT mice, LPS challenge caused systemic hypotension, a significantly blunted vasoconstrictor response to norepinephrine, and an impaired endothelium-dependent vasodilator response to acetylcholine, concomitant with a markedly increased aortic inducible NO synthase expression, significantly elevated plasma and aortic levels of nitrite/nitrate, increased aortic TNF-alpha expression, and decreased aortic endothelial NO synthase (eNOS) expression.

Activation of endothelial intrinsic NF-{kappa}B pathway impairs protein C anticoagulation mechanism and promotes coagulation in endotoxemic mice.

Although the role of systemic activation of the nuclear factor kappaB (NF-kappaB) pathway in septic coagulation has been well documented, little is known about the contribution of endothelial-specific NF-kappaB signaling in this pathologic process. Here, we used transgenic mice that conditionally overexpress a mutant I-kappaBalpha, an inhibitor of NF-kappaB, selectively on endothelium, and their wild-type littermates to define the role of endothelial-specific NF-kappaB in septic coagulation. In wild-type mice, lipopolysaccharide (LPS) challenge (5 mg/kg intraperitoneally) caused markedly increased plasma markers of coagulation, decreased plasma fibrinogen level, and widespread tissue fibrin deposition, which were abrogated by endothelial NF-kappaB blockade in transgenic mice.

Divergent roles of endothelial NF-kappaB in multiple organ injury and bacterial clearance in mouse models of sepsis.

To define the roles of endothelial-intrinsic nuclear factor kappaB (NF-kappaB) activity in host defense and multiple organ injury in response to sepsis, we generated double transgenic (TG) mice (EC-rtTA/I-kappaB alpha mt) that conditionally overexpress a degradation-resistant form of the NF-kappaB inhibitor I-kappaB alpha (I-kappaB alpha mt) selectively on vascular endothelium. The EC-rtTA/I-kappaB alpha mt mice had no basal, but a relatively high level of doxycycline-inducible, I-kappaB alpha mt expression. I-kappaB alpha mt expression was detected in endothelial cells, but not in fibroblasts, macrophages, and whole blood cells, confirming that transgene expression was restricted to the endothelium.