SummaryLong non-coding RNAs (lncRNAs) are increasingly recognized as important regulators in tumor development. This study aims to investigate the potential role oflncRNALEF1-AS1, in the progression of lung cancer. Quantitative real-time PCR (qRT-PCR) and western blot assays showed that LEF1-AS1 was upregulated while miR-544a was downregulated in lung cancer specimens and cells. Overexpression of LEF1-AS1 led to the enhancement of cell proliferation and invasion, revealed by CCK-8 assay and transwell assay. A negative correlation was found between LEF1-AS1 and miR-544a. BLAST analysis and dual-luciferase assay confirmed that FOXP1 is a downstream effector of miR-544a. Therefore, the LEF1-AS1/miR-544a/FOXP1 axis is an important contributor to lung cancer progression. Collectively, our novel data uncovers a new mechanism that governs tumor progression in lung cancer and provides new targets that may be used for disease monitoring and therapeutic intervention of lung cancer.
The transforming growth factor β regulator 4 (TBRG4) gene, located on the 7p14-p13 chromosomal region, is implicated in numerous types of cancer. However, the contribution(s) of TBRG4 in human lung cancer remains unknown. In the present study, the expression of TBRG4 mRNA was investigated in the H1299 lung cancer cell line using the quantitative polymerase chain reaction (qPCR) following the knockdown of TBRG4 by a lentivirus-mediated small interfering RNA (siRNA). Results identified that the expression of TBRG4 within H1299 cells was significantly suppressed (P<0.01) by RNA interference, and 586 genes were differentially expressed following TBRG4 silencing. Ingenuity Pathway Analysis (IPA) revealed that these genes were often associated with infectious diseases, organismal injury, abnormalities and cancer functional networks. Further IPA of these networks revealed that TBRG4 knockdown in H1299 cells deregulated the expression of 21 downstream genes, including the upregulation of DNA damage-inducible transcript 3 (DDIT3), also termed CCAAT/enhancer-binding protein homologous protein, and downregulation of caveolin 1 (CAV1) and ribonucleotide reductase regulatory subunit M2 (RRM2). Results were validated using qPCR and western blotting. Furthermore, immunohistochemical staining of TBRG4 protein identified that expression was markedly increased in carcinoma compared with in normal tissue. In conclusion, TBRG4 serves a role in the tumorigenesis of lung cancer via deregulation of DDIT3, CAV1 and RRM2. The results of the present study may be important in contributing to our understanding of TBRG4 as a target for lung cancer treatment.
Abstract. The current study examined the role of Raf kinase inhibitor protein (RKIP) in non-small cell lung cancer (NSCLC) metastasis. A total of 100 patients with NSCLC were recruited following pathological diagnosis in the First Affiliated Hospital of Bengbu Medical College. The patients were classified and statistically analyzed according to their clinicopathological characteristics and tumor-node-metastasis stage. Paired tumor tissue and adjacent non-tumor tissue samples were subject to pathological diagnosis and western blot analysis. Transient transfection and lentivirus particle vector-mediated RKIP overexpression, small interfering RNA-mediated silencing, Transwell assays and immunocytochemistry methods were employed to elucidate the role and underlying mechanisms of RKIP and the Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling pathway in NSCLC metastasis. Furthermore, in order to examine the in vivo effects of RKIP, recombinant lentivirus particles containing the RKIP gene were administrated in a mouse NSCLC tumor model via tail vein injection. The results revealed reduced RKIP expression levels in NSCLC tissue compared with corresponding non-cancer tissue. Additionally, RKIP expression levels were inversely associated with NSCLC intra-lung, lymph node and long-distance metastasis. The results also indicated that RKIP was able to block STAT3 activation via phosphorylation and inhibit NSCLC-cell metastasis in vitro. Furthermore, RKIP knockdown was able to promote STAT3 phosphorylation and cell metastasis in NSCLC cell lines. During in vivo experiments, RKIP overexpression was able to suppress xenograft tumor metastasis in nude mice. Therefore, RKIP may be an important factor in cancer cell metastasis in patients with NSCLC, and RKIP may inhibit NSCLC-cell invasion by blocking the activation of the JAK/STAT3 signaling pathway. IntroductionLung cancer has increased in incidence in the developing world since 2008, from 1.8 to 2 million per year, and this trend is predicted to continue in the future (1). Non-small cell lung cancer (NSCLC) is among the most malignant types of cancer, and has a high mortality rate (2). Approximately 80-90% of lung cancer cases are of NSCLC, and 50-70% of these patients are diagnosed at the advanced stage of disease (1,3). The survival time of patients with lung cancer is 5 years in 10-15% of cases, with the remaining exhibiting poorer survival times (1). Therefore, the early prevention of NSCLC metastasis is a key factor in lung cancer prevention and the development of novel therapeutic agents. A number of studies have investigated the mechanisms underlying NSCLC metastasis (4,5); however, the exact mechanisms underlying this process require further elucidation.Raf kinase inhibitor protein (RKIP) is a small evolutionarily conserved protein, which was initially identified to function as a physiological inhibitor of the Raf/mitogen-activated protein kinase kinase (MEK)/extracellular signal-regulated kinase (ERK) signaling pathway (6). RKIP inhib...
Although canine adenovirus (CAdV) is highly prevalent in dogs, there is currently a lack of a quick diagnostic method. In this study, we developed a rapid immunochromatographic strip (ICS) assay using colloidal gold coupled to CAdV-2-specific monoclonal antibodies (mAbs). BALB/c mice were immunized with a purified CAdV-2 suspension, and four mAbs (belonging to two different epitopes) were generated and designated as 2C1, 7D7, 10D1, and 4G1. Western blot and protein spectral analysis indicated that the hexon protein of CAdV-2 recognized all four mAbs. The colloidal gold-coupled 7D7 and 2C1 mAbs were chosen for inclusion in the rapid ICS assay. The optimal concentrations of the coating antibody (2C1), the capture antibody (7D7), and the goat anti-mouse antibody were 1.0 mg/ml, 10 µg/ml, and 2.0 mg/ml, respectively. The limit of detection was approximately 2.0 × 10 2 tissue culture infective dose (TCID 50 )/ml. Other common canine viruses were tested to evaluate the specificity of the ICS, and positive results were observed for only CAdV-1 and CAdV-2. The ICS test was conducted on 360 samples to detect CAdV, and the results were compared with those of polymerase chain reaction (PCR) tests. The ICS test was found to be a sufficiently sensitive and specific detection method for the convenient and rapid detection of CAdV.
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