Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0345904 (liver cancer)
 15,188 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Evidence indicates that exposure to heavy trace element might be a risk factor for liver carcinoma. Cadmium has been supposed to be a carcinogen that has a correlation with the risk of a number of cancers, including liver cancer. However, the mechanisms underlying Cadmium-induced malignant transformation in liver cells are not fully understood. In the present study, we aimed to screen the differentially expressed genes (DEGs) that might play a role in both the Cadmium-related liver cell transformation and the development of liver cancer. Microarray-based gene expression profiles concerning liver carcinoma vs non-cancerous tissue (GSE64041) and Cadmium-treated liver cells vs controls (GSE8865 and GSE31286), respectively, were retrieved from Gene Expression Omnibus (GEO) database. Then, DEGs of each profile were calculated and screened. The intersection of each DEGs was obtained by Venn analysis. Afterwards, the possible roles of the selected genes in cancer development were evaluated by using Oncomine database and TCGA cohort analysis. Consequently, three DEGs, LRAT, SLC7A11, and ITGA2, were selected for further analysis. SLC7A11 and ITGA2, but not LRAT, were upregulated in liver cancer compared with those in normal tissues, respectively. After using a TCGA cohort analysis, results failed to show a significant correlation between SLC7A11 or ITGA2 expression and clinical parameters. However, the survival analysis showed that patients with high expression levels of SLC7A11 had a shorter overall survival time relative to those of the patients with low levels. In conclusion, SLC7A11 and ITGA2 might play a role in the Cadmium-induced liver cell damage or transformation, and the development of liver carcinoma. SLC7A11 might be a prognostic factor for patients with liver carcinoma. Future validation experiments are needed to verify the results.
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PMID:Identification and Characterization of Cadmium-Related Genes in Liver Carcinoma. 2879 17

Hepatocellular carcinoma (HCC) is a leading cause of cancer-related death. The aim of this study was to identify underlying hub genes and dysregulated pathways associated with the development of HCC using bioinformatics analysis. Differentially expressed protein-coding genes were subjected to transcriptome sequencing in 11 pairs of liver cancer tissue and matched adjacent non-cancerous tissue. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed, followed by protein-protein interaction (PPI) network construction. Hub genes were identified via centralities analysis and verified using published datasets. In total, 720 significantly differentially expressed protein-coding genes were identified in the samples, including 335 upregulated genes and 385 downregulated genes. The upregulated genes were significantly enriched in cell adhesion, biological adhesion and cell-cell adhesion GO terms under biological process (BP). Conversely, the downregulated genes were significantly enriched in embryonic organ morphogenesis, embryonic organ development and embryonic morphogenesis. The KEGG pathway analysis showed that the upregulated genes were enriched in ECM-receptor interaction and focal adhesion pathways. Furthermore, the downregulated genes were enriched in the ErbB, VEGF and MAPK signaling pathways. The PPI network and centralities analysis suggested that ITGA2 and 12 alternate genes were significant hub genes. These findings improve current understanding of the molecular mechanisms underlying HCC development and may be helpful in identifying candidate molecular biomarkers for use in diagnosing, treating and monitoring the prognosis of HCC.
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PMID:Identification of hub genes involved in the development of hepatocellular carcinoma by transcriptome sequencing. 2894 76

ITGA2 (Integrin alpha-2) has been detected to be over-expressed in a number of cancers and has been suggested to be involved in cell adhesion and cell-surface mediated signaling. Our previous study using bioinformatic analyses has shown that ITGA2 might be a key gene being involved in the Cadmium-induced malignant transformation of liver cells. In the present study, we firstly aimed to learn the possible functions of ITGA2 via bioinformatics analysis, and then test its expression and clinical significance in liver carcinoma specimens through laboratory experiments. Gene ontology (GO) and pathway enrichment analysis, as well as protein-protein interaction (PPI) analysis has been conducted in Genecards. Then, a tissue microarray containing 90 cases of liver cancer and 90 paired adjacent non-cancerous samples was used for detection of ITGA2 expression by immunohistochemistry assay. Consequently, ITGA2 may be enriched in pathways regarding cell adhesion and migration. PPI analysis suggests that ITGA1, ITGB2, FLT4, LAMB1 and AGRN may have a close relationship with ITGA2. No association between ITGA2 expression and clinical parameters was observed. However, the data showed that ITGA2 might be an independent prognostic factor for liver cancer patients. In conclusion, the data suggest that ITGA2 over-expression might be a potential unfavorable prognostic factor and a potential therapeutic target for liver carcinoma.
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PMID:Is Integrin Subunit Alpha 2 Expression a Prognostic Factor for Liver Carcinoma? A Validation Experiment Based on Bioinformatics Analysis. 3051 39