Isolation of anti-tumor monoclonal antibodies targeting on MICA/B α3 domain by single B cell technology for colon cancer therapy.

Colon cancer (CC) is one of the most common gastrointestinal malignancies. Effectiveness of the existing therapies is limited. Immunotherapy is a promising complementary treatment approach for CC.

Brain-derived neurotrophic factor promotes airway smooth muscle cell proliferation in asthma through regulation of transient receptor potential channel-mediated autophagy.

Objective: Increased proliferation of airway smooth muscle cells (ASMCs) is a key feature of airway remodeling in asthma. This study aims to determine whether brain-derived neurotrophic factor (BDNF) regulates ASMC proliferation and airway remodeling via the transient receptor potential channels (TRPCs)/autophagy axis.

Methods: Human ASMCs were isolated and passively sensitized with human asthmatic serum.

Amygdalin alleviated TGF-β-induced epithelial-mesenchymal transition in bronchial epithelial cells.

Objective: Transforming growth factor-beta TGF-β-induced epithelial-mesenchymal transition (EMT) in bronchial epithelial cells contributes to airway wall remodeling in asthma. This study aims to explore the role of amygdalin, an active ingredient in bitter almonds, in TGF-β-induced EMT in bronchial epithelial cells and to elucidate the possible mechanisms underlying its biological effects.

Methods: An asthmatic mouse model was established through ovalbumin induction.

SRSF1 promotes ASMC proliferation in asthma by competitively binding CCND2 with miRNA-135a.

Background: Asthma is an inflammatory syndrome characterized by airway hyperresponsiveness, bronchial inflammation, and airway remodeling. Abnormal proliferation of airway smooth muscle cells (ASMCs) is the main pathological feature of asthma. This study investigated the function and mechanism of serine arginine-rich splicing factor 1 (SRSF1) in ASMC proliferation in asthma.

Exosomal transfer of activated neutrophil-derived lncRNA CRNDE promotes proliferation and migration of airway smooth muscle cells in asthma.

Activated neutrophil-derived exosomes reportedly contribute to the proliferation of airway smooth muscle cells (ASMCs), thereby aggravating the airway wall remodeling during asthma; however, the specific mechanism remains unclear. Lipopolysaccharide (LPS)-EXO and si-CRNDE-EXO were extracted from the media of human neutrophils treated with LPS and LPS + si-CRNDE (a siRNA targets long non-coding RNA CRNDE), respectively. Human ASMCs were co-cultured with LPS-EXO or si-CRNDE-EXO, and cell viability, proliferation and migration were measured.

LincRNA-p21 promotes classical macrophage activation in acute respiratory distress syndrome by activating NF-κB.

Previous studies have revealed the important role of alveolar macrophages (AMs) in the pathogenesis of acute respiratory distress syndrome (ARDS) and potential anti-inflammatory properties of lincRNA-p21. This study aims to study the association between lincRNA-p21 and active AMs to understand the molecular mechanisms of AMs-mediated inflammatory responses in ARDS. This study was mainly investigated in mice with the intratracheal instillation of lipopolysaccharide (LPS) or LPS-treated AMs.

Involvement of E-cadherin/AMPK/mTOR axis in LKB1-induced sensitivity of non-small cell lung cancer to gambogic acid.

Liver kinase B1 (LKB1) is a tumor suppressor that functions as master regulator of cell growth, metabolism, survival, and polarity. Patients with NSCLC possessing mutated LKB1 respond to chemotherapy differently from those with wild-type LKB1. Gambogic acid (GA), a small molecule from natural product, has been established as an anti-tumor agent due to its potent activity and low toxicity.

Diagnostic accuracy of serum dickkopf-1 protein in diagnosis hepatocellular carcinoma: An updated meta-analysis.

Background: To verify the accuracy of serum dickkopf-1 protein (DKK-1) in the diagnosis of hepatocellular carcinoma (HCC) by an updated meta-analysis.

Methods: We searched potential eligible studies in PubMed and Embase before July 8, 2018. Sensitivity (SN), specificity (SP), positive likelihood ratio (PLR), negative likelihood ratio (NLR), summary receiver operating characteristics curve (sROC), and diagnostic odds ratio (DOR) were pooled with their 95% confidence intervals CIs) using a bivariate random-effects model.

Upregulated microRNA miR-21 promotes the progression of lung adenocarcinoma through inhibition of KIBRA and the Hippo signaling pathway.

Purpose: In this study, we aimed to identify the key pathways and hub genes in lung adenocarcinoma (LAD) through bioinformatics analysis and to identify the miRNAs that targeted the selected hub gene. The present study was conducted to explore the effect of the hub gene KIBRA, the Hippo signaling pathway and miR-21 on LAD progression.

Methods: Through gene set enrichment analysis (GSEA), the enriched KEGG pathways involved in LAD were identified.

GAS5 promotes airway smooth muscle cell proliferation in asthma via controlling miR-10a/BDNF signaling pathway.

Aims: To explore the role of long non-coding RNA (lncRNA) growth arrest-specific transcript 5 (GAS5) in the cell proliferation of airway smooth muscle cells (ASMCs) in asthma.

Materials And Methods: An asthma rat model was established by ovalbumin sensitization and challenge. The expression of GAS5, miR-10a and BDNF mRNA and protein was determined with qRT-PCR and western blot, separately.

The effects of transient receptor potential channel (TRPC) on airway smooth muscle cell isolated from asthma model mice.

This study aimed to validate whether transient receptor potential channel1 (TRPC1) and TRPC3 participate in the regulation the proliferation of airway smooth muscle cells (ASMCs) through modulating calcium ion (Ca ) influx in vitro. Chronic model of murine asthma was induced and ASMCs isolated from asthmatic mice were used in this whole study. TRPC1 and TRPC3 were upregulated in asthmatic mouse ASMCs and selected for further investigation.

Schisandrin B down-regulated lncRNA BCYRN1 expression of airway smooth muscle cells by improving miR-150 expression to inhibit the proliferation and migration of ASMC in asthmatic rats.

Objective: The mechanism of Schisandrin B on the proliferation and migration of airway smooth muscle cells (ASMCs) in asthmatic rats was explored.

Methods: SD rats were divided into three groups: control (group 1), model (group 2) and model + Schisandrin B (group 3). miR-150 and lncRNA BCYRN1 levels were measured by qRT-PCR.

LncRNAs BCYRN1 promoted the proliferation and migration of rat airway smooth muscle cells in asthma via upregulating the expression of transient receptor potential 1.

Background: Long noncoding RNAs (lncRNAs) played important roles in several biological processes through regulating the expression of protein. However, the function of lncRNA BCYRN1 in airway smooth muscle cells (ASMCs) has not been reported.

Methods: Male Sprague-Dawley (SD) rats were divided into control and asthma groups and the ovalbumin (OVA) model was constructed.

Schisandrin B inhibits the proliferation of airway smooth muscle cells via microRNA-135a suppressing the expression of transient receptor potential channel 1.

Airway smooth muscle cell (ASMC) was known to involve in the pathophysiology of asthma. Schisandrin B was reported to have anti-asthmatic effects in a murine asthma model. However, the molecular mechanism involving in the effect of Schisandrin B on ASMCs remains poorly understood.