Exploration of potential biomarkers involved in acute myocardial infarction
INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL MEDICINE
Authors: Wu, Yingbiao; Fang, Ming; Luo, Jun; Jin, Can; Hao, Shuwen; Tian, Bei; Fang, Chao; Li, Xinming; Ning, Zhongping
Abstract
Objective: The aim of the current study was to screen potential novel biomarkers involved in AMI. Methods: Microarray data of AMI (GSE66360) was obtained from the Gene Expression Omnibus (GEO) database. Usingthe limma package, differentially-expressed genes (DEGs) between samples from AMI and healthy controls were screened. Based on the DAVID tool, functional analysis was carried out Protein-protein interaction (PPI) and transcription factor (TF)-miRNA-target gene regulatory networks were visualized using Cytoscape software. Finally, drug gene interactions were predicted using the DGIdb database. Results: A total of 339 DEGs between samples from AMI and healthy controls were identified. Upregulated DEGs were mainly enriched in 32 pathways, including osteoclast differentiation, TNF signaling pathways, and transcriptional mis regulation in cancer. Cytokine-cytokine receptor interaction was the main functional enrichment for downregulated DEGs. IL8, JUN, IL1B, TNF, and FOS were key nodes in the PPI network. In addition, three miRNAs, including has-miR-191, has-miR-101, and has-miR-20, nine TFs, including NFKAPPAB, SRF, IK3, and NFKAPPAB65, and 34 regulatory relationship pairs were integrated. Prediction results revealed that TNF, IL1B, and TLR4 might be potential druggable genes for AMI patients. Conclusion: IL8, JUN, IL1B might be novel markers for atherosclerotic plaque instability. MicroRNAs, including miR-191, miR-101, and miR-20, might provide a window for exploration of potential biomarkers for diagnosis and prognosis for AMI patients.
Increasing Incidence of Colon Cancer in the Young: Assessing the Tumor Biology
JOURNAL OF THE AMERICAN COLLEGE OF SURGEONS
Authors: Nfonsam, Valentine N.; Jecius, Hunter; Chen, Debbie; Omesiete, Pamela N.; Ewongwo, Agnes N.; Elquza, Emad; Scott, Aaron J.; Jandova, Jana
Abstract
BACKGROUND: The overall incidence of colon cancer (CC) is decreasing, but with increasing early-onset colon cancer (EOCC < 50 years old). Our recent study revealed unique overexpression of cartilage oligomeric matrix protein (COMP) in EOCC and its association with aggressiveness. The aim of this study was to assess CC biology, especially in the young, by evaluating the role of COMP in CC carcinogenesis and cancer progression, detecting COMP in serum and its association with disease stage. STUDY DESIGN: Cancer and matching noninvolved tissue blocks from 12 sporadic EOCC and late-onset colon cancer (LOCC) patients of 4 disease stages were obtained from pathology archives. Ribonucleic acid expression profiling of 770 cancer-related genes using nCounter platform was performed. The COMP levels from 16 EOCC and LOCC serum samples were measured by ELISA. Carcinoembryonic antigen levels from these 16 samples were taken at the time of diagnosis. Transwell assay was performed to elucidate the role of COMP in motility and metastases. RESULTS: Expression profiling revealed increased COMP levels in higher disease stage. There was 7-fold higher COMP expression (p <= 0.05) in stage III compare to stage I and its coexpression with GAS1, VEGFC, MAP3K8, SFRP1, and PRKACA. Higher COMP expression was seen in stage II compared with stage I (p = 0.07) and its coexpression with TLR2, IL8, RIN1, IRAK3, and CACNA2D2, and COMP was detectable in serum and showed significantly higher levels in EOCC compared with LOCC. Similar correlation was seen with CEA levels, but the difference was not significant. Transwell assay revealed significantly increased motility of HT-29 cells after treatment with recombinant COMP. CONCLUSIONS: These findings suggest different tumor biology between EOCC and LOCC. Cartilage oligomeric matrix protein plays a significant role in CC carcinogenesis and has potential as biomarker for CC, especially aggressive EOCC. ((C) 2019 by the American College of Surgeons. Published by Elsevier Inc. All rights reserved.)