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)

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

Despite the critical position of translation in the multilevel gene expression regulation program, high-resolution and genome-wide view of the landscape of RNA translation in solid tumors is still limited. Methods: With a ribosome profiling procedure optimized for solid tissue samples, we profiled the translatomes of liver tumors and their adjacent noncancerous normal liver tissues from 10 patients with hepatocellular carcinoma (HCC). A set of bioinformatics tools was then applied to these data for the mining of novel insights into the translation shifts in HCC. Results: This is the first translatome data resource for dissecting dysregulated translation in HCC at the sub-codon resolution. Based on our data, quantitative comparisons of mRNA translation rates yielded the genes and processes that were subjected to patient specific or universal dysregulations of translation efficiencies in tumors. For example, multiple proteins involved in extracellular matrix organization exhibited significant translational upregulation in tumors. We then experimentally validated the tumor-promoting functions of two such genes as examples: AGRN and VWA1. In addition, the data was also used for de novo annotation of the translatomes in tumors and normal tissues, including multiple types of novel non-canonical small ORFs, which would be a resource for further functional studies. Conclusions: The present study generates the first survey of the HCC translatome with ribosome profiling, which is an insightful data resource for dissecting the translatome shift in liver cancer, at sub-codon resolution.
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PMID:Survey of the translation shifts in hepatocellular carcinoma with ribosome profiling. 3128 37