ABSTRACT
PROPOSE: We aimed to explore the potential molecular mechanism and independent prognostic genes for colon cancer (CC). METHODS: Microarray datasets GSE17536 and GSE39582 were downloaded from Gene Expression Omnibus. Meanwhile, the whole CC-related dataset were downloaded from The Cancer Genome Atlas (TCGA) database. Differentially expressed mRNA (DEMs) were identified between cancer tissue samples and para-carcinoma tissue samples in TCGA dataset, followed by the KEGG pathway and GO function analyses. Furthermore, the clinical prognostic analysis including overall survival (OS) and disease-free survival (DFS) were performed in all three datasets. RESULTS: A total of 633 up- and 321 down-regulated mRNAs were revealed in TCGA dataset. The up-regulated mRNAs were mainly assembled in functions including extracellular matrix and pathways including Wnt signaling. The down-regulated mRNAs were mainly assembled in functions like Digestion and pathways like Drug metabolism. Furthermore, up-regulation of UL16-binding protein 2 (ULBP2) was associated with OS in CC patients. A total of 12 DEMs including Surfactant Associated 2 (SFTA2) were potential DFS prognostic genes in CC patients. Meanwhile, the GRP and Transmembrane Protein 37 (TMEM37) were two outstanding independent DFS prognostic genes in CC. CONCLUSIONS: ULBP2 might be a potential novel OS prognostic biomarker in CC, while GRP and TMEM37 could be served as the independent DFS prognostic genes in CC. Furthermore, functions including extracellular matrix and digestion, as well as pathways including Wnt signaling and drug metabolism might play important roles in the process of CC.
Subject(s)
Humans , Animals , Colonic Neoplasms/diagnosis , Colonic Neoplasms/genetics , Gene Expression Profiling/methods , RNA, Messenger/genetics , RNA, Messenger/metabolism , Biomarkers, Tumor/genetics , Biomarkers, Tumor/metabolism , Genetic Markers , Down-Regulation/genetics , Gene Expression Regulation, Neoplastic , Up-Regulation/genetics , Risk Factors , Colonic Neoplasms/metabolism , Disease-Free Survival , Gastrin-Releasing Peptide/genetics , Gastrin-Releasing Peptide/metabolism , Intercellular Signaling Peptides and Proteins/genetics , Intercellular Signaling Peptides and Proteins/metabolism , Pulmonary Surfactant-Associated Protein A/genetics , Pulmonary Surfactant-Associated Protein A/metabolism , Microarray Analysis , Murinae , Kaplan-Meier Estimate , GPI-Linked Proteins/genetics , GPI-Linked Proteins/metabolismABSTRACT
PURPOSE: To evaluate surfactant protein A levels in an hepatopulmonary syndrome rat model. To date, there have been no studies aimed at evaluating surfactant levels in the setting of cirrhosis or hepatopulmonary syndrome. METHODS: A total of 35 rats were divided into control, sham, and experimental HPS groups. We evaluated surfactant protein A levels in rats and the experimental model designed to induce hepatopulmonary syndrome was common bile duct ligation. Statistical analysis was performed using GraphPad Prism Software(r). Differences were considered statistically significant when p<0.05. RESULTS: Lung homogenate of surfactant protein A levels were lower in the experimental hepatopulmonary syndrome and sham groups in comparison to the control group (p<0.05). Serum SP-A levels were the same in experimental hepatopulmonary syndrome and control groups but decreased in the sham group compared with the experimental groups (p<0.05). Myeloperoxidase activity was higher in the experimental hepatopulmonary syndrome group than the other two groups (p<0.05). CONCLUSION: Surfactant protein A is present in experimental hepatopulmonary syndrome and leads to an imbalance between serum and pulmonary levels due to systemic inflammatory response. .
Subject(s)
Animals , Male , Disease Models, Animal , Hepatopulmonary Syndrome/metabolism , Lung/metabolism , Pulmonary Surfactant-Associated Protein A/metabolism , Blood Gas Analysis , Common Bile Duct , Hepatopulmonary Syndrome/pathology , Ligation , Peroxidase/metabolism , Pulmonary Surfactant-Associated Protein A/analysis , Rats, Wistar , Reference ValuesABSTRACT
BACKGROUND & OBJECTIVES: The decrease in surfactant protein-A (SP-A level) has recently been implicated in the pathophysiology of acute respiratory distress syndrome (ARDS). Mechanical ventilation is the main modality of treatment of ARDS. But information on the SP-A levels after mechanical ventilation is scanty. We therefore studied the effect of mechanical ventilation on SP-A levels in patients with ARDS. METHODS: In a prospective, observational study conducted in the Respiratory Intensive Care Unit of a tertiary care hospital in north India, 13 patients with ARDS requiring mechanical ventilation were included. SP-A levels in the bronchial aspirates were serially estimated by ELISA at the start of mechanical ventilation and after 24 and after 48 h. RESULTS: The SP-A level at the start of mechanical ventilation was 3.06 +/- 2.56 microg/ml. The levels gradually increased to 3.99 +/- 2.39 and 6.64 +/- 2.72 microg/ml, at 24 and 48 h respectively, and this increase was statistically significant (P < 0.05). Patients having an infectious etiology had lower SP-A levels compared to those with non-infections causes. Neither the initial SP-A level nor the increase in SP-A level correlated with the improvement in lung function or duration of ventilation. INTERPRETAION & CONCLUSION: The present study showed a progressive increase in the SP-A levels in patients with ARDS on mechanical ventilation. Further studies are required to confirm that the increase in SP-A levels may be one of the contributors for recovery in ARDS.