Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017638 (glioma)
 30,880 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Coronins have maintained a high degree of conservation over the roughly 800 million years of eukaryotic evolution.1,2 From its origins as a single gene in simpler eukaryotes, the mammalian Coronin gene family has expanded to include at least six members (see Chapter 4). Increasing evidence indicates that Coronins play critical roles as regulators of actin dependent processes such as cell motility and vesicle trafficking3,4 (see Chapters 6-9). Considering the importance of these processes, it is not surprising that recent findings have implicated the involvement of Coronins in multiple diseases. This review primarily focuses on Coronin 1C (HGNC symbol: CORO1C, also known as Coronin 3) which is a transcriptionally dynamic gene that is up-regulated in multiple types of clinically aggressive cancer. In addition to reviewing the molecular signals and events that lead to Coronin 1C transcription, we summarize the results of several studies describing the possible functional roles of Coronin 1C in development as well as disease progression. Here, the main focus is on brain development and on the progression of melanoma and glioma. Finally, we will also review the role of other mammalian Coronin genes in clinically relevant processes such as neural regeneration and pathogenic bacterial infections (see Chapter 10).
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PMID:The role of mammalian coronins in development and disease. 1892 77

Brain-enriched miR-128 is repressed in glioma cells, and could inhibit the proliferation of gliomas by targeting genes such as E2F3a and BMI1. To identify more targets of miR-128 in glioblastoma multiforme, the pulse stable isotope labeling with amino acids in cell culture (pSILAC) technique was used to test its impact on whole protein synthesis in T98G glioma cells. We successfully identified 1897 proteins, of which 1459 proteins were quantified. Among them, 133 proteins were downregulated after the overexpression of miR-128. Through predictions using various bioinformatics tools, 13 candidate target genes were chosen. A luciferase assay validated that 11 of 13 selected genes were potential targets of miR-128, and a mutagenesis experiment confirmed CBFB, CORO1C, GLTP, HnRNPF, and TROVE2 as the target genes. Moreover, we observed that the expression of CORO1C, TROVE2, and HnRNPF were higher in glioma cell lines compared to normal brain tissues and presented a tendency toward downregulation after overexpression of miR-128 in T98G cells. Furthermore, we have validated that CORO1C, TROVE2, and HnRNPF could inhibit glioma cell proliferation. In sum, our data showed that the integration of pSILAC and bioinformatics analysis was an efficient method for seeking the targets of miRNAs, and plentiful targets of miR-128 were screened and laid the foundation for research into the miR-128 regulation network.
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PMID:Proteomic screening and identification of microRNA-128 targets in glioma cells. 2578 Dec 72