Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.7.6 (RNA polymerase)
 34,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Malignant melanoma is one of the most common types of cancer worldwide. Efforts have been made to elucidate the pathology of malignant melanoma. However, its molecular mechanisms remain unclear. Therefore, the microarray datasets GSE3189, GSE4570 and GSE4587 from the Gene Expression Omnibus database were used for the elucidation of candidate genes involved in the initiation and progression of melanoma. Assessment of the microarray datasets led to the identification of differentially expressed genes (DEGs), which were subsequently used for function enrichment analysis. These data were utilized in the construction of the protein-protein interaction network and module analysis was conducted using STRING and Cytoscape software. The results of these analyses led to the identification of a total of 182 DEGs, including 52 downregulated and 130 upregulated genes. The functions and pathways found to be enriched in the DEGs were GTPase activity, transcription from RNA polymerase II promoter, apoptotic processes, cell adhesion, membrane related pathways, calcium signaling cascade and the PI3K-Akt signaling pathway. The identified genes were demonstrated to belong to a set of 10 hub genes biologically involved in proliferation, apoptosis, cytokinesis, adhesion and migration. Survival analysis and Oncomine database analysis revealed that the calmodulin gene family, BAX and VEGFA genes, may be associated with the initiation, invasion or recurrence of melanoma. In conclusion, the DEGs and hub genes identified in the present study may be used to understand the molecular pathways involved in the initiation and progression of malignant melanoma. Furthermore, the present study may aid in the identification of possible targets for the diagnosis and treatment of melanoma.
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PMID:Identification of prognostic biomarkers for malignant melanoma using microarray datasets. 3162 Jan 97

The senescence response to oncogenes is believed to be a barrier to oncogenic transformation in premalignant lesions, and describing the mechanisms by which tumor cells evade this response is important for early diagnosis and treatment. The male germ cell-associated protein SSX2 is ectopically expressed in many types of cancer and is functionally involved in regulating chromatin structure and supporting cell proliferation. Similar to many well-characterized oncogenes, SSX2 has the ability to induce senescence in cells. In this study, we performed a functional genetic screen to identify proteins implicated in SSX2-induced senescence and identified several subunits of the Mediator complex, which is central in regulating RNA polymerase-mediated transcription. Further experiments showed that reduced levels of MED1, MED4, and MED14 perturbed the development of senescence in SSX2-expressing cells. In contrast, knockdown of MED1 did not prevent development of B-Raf- and Epirubicin-induced senescence, suggesting that Mediator may be specifically linked to the cellular functions of SSX2 that may lead to development of senescence or be central in a SSX2-specific senescence response. Indeed, immunostaining of melanoma tumors, which often express SSX proteins, exhibited altered levels of MED1 compared to benign nevi. Similarly, RNA-seq analysis suggested that MED1, MED4, and MED14 were downregulated in some tumors, while upregulated in others. In conclusion, our study reveals the Mediator complex as essential for SSX2-induced senescence and suggests that changes in Mediator activity could be instrumental for tumorigenesis.
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PMID:A functional genetic screen identifies the Mediator complex as essential for SSX2-induced senescence. 3169 25


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