Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.25.1 (deoxyribonuclease)
 1,471 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cytolethal distending toxin (CDT) is a secreted tripartite genotoxin produced by many pathogenic gram-negative bacteria. It is composed of three subunits, CdtA, CdtB and CdtC, and CdtB-associated deoxyribonuclease (DNase) activity is essential for the CDT toxicity. In the present study, to design a novel potentially antitumor drug against lung cancer, the possible mechanisms of cdtB anticancer properties were explored in the A549 human lung adenocarcinoma cell line. A recombinant plasmid pcDNA3.1/cdtB was constructed expressing CdtB of human periodontal bacterium Aggregatibacter actinomycetemcomitans and investigated for toxic properties in A549 cells and possible mechanisms. It was observed that plasmid pcDNA3.1/cdtB caused loss of cell viability, morphologic changes and induction of apoptosis. Furthermore, measurement of caspase activity indicated involvement of an intrinsic pathway of cell apoptosis. Consequently, the recombinant plasmid pcDNA3.1/cdtB may have potential as a new class of therapeutic agent for gene therapy of lung cancer.
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PMID:Apoptotic Effects of the B Subunit of Bacterial Cytolethal Distending Toxin on the A549 Lung Cancer Cell Line. 2716 42

Non-small-cell lung cancer (NSCLC) is the most common cause of cancer-associated mortality worldwide. MicroRNAs (miRs) are a class of small non-coding RNAs that are commonly dysregulated in human cancer. The aim of the current study was to evaluate the effect of miR-296-3p on the cell migration and invasion of NSCLC. Pairs of tumor tissues and para-cancerous tissues (n=50) were collected from patients with NSCLC, and the expression of miR-296-3p was analyzed by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Additionally, tumor cell viability, migration and invasion were examined in vitro using Cell Counting Kit-8, wound healing and Matrigel assays, respectively. Furthermore, potential targets of miR-296-3p were screened for using TargetScan and validated using a dual-luciferase reporter assay. The expression levels of phosphoinositide-3-kinase (PI3K), AKT serine/threonine kinase (AKT), mammalian target of rapamycin (mTOR), matrix metallopeptidase 2 (MMP2) and SRY-box 4 (SOX4) were detected by RT-qPCR and western blot analysis. The data indicated that miR-296-3p was downregulated in tumor tissues compared with adjacent normal tissues. Overexpression of miR-296-3p inhibited NSCLC cell viability, migration and invasion in vitro. Furthermore, apurinic/apyrimidinic endodeoxyribonuclease 1 (APEX1) was identified as a direct target of miR-296-3p. APEX1 expression was upregulated in tumor tissues compared with para-cancerous tissues, and the mRNA and protein expression levels of APEX1 were decreased following transfection of NSCLC cells with miR-296-3p mimics compared with control cells. Additional investigations revealed that miR-296-3p was involved in regulating the PI3K/AKT/mTOR signaling pathway, and miR-296-3p mimics decreased the mRNA and protein expression levels of MMP2 and SOX4. In summary, the findings demonstrated that miR-296-3p may function as a tumor suppressor, and inhibits the migration and invasion of NSCLC cells by targeting APEX1. miR-296-3p is therefore a potential therapeutic molecular modulator of NSCLC.
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PMID:miR-296-3p targets APEX1 to suppress cell migration and invasion of non-small-cell lung cancer. 3140 54