| pubmed-article:21779463 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:21779463 | lifeskim:mentions | umls-concept:C0006826 | lld:lifeskim |
| pubmed-article:21779463 | lifeskim:mentions | umls-concept:C1101610 | lld:lifeskim |
| pubmed-article:21779463 | lifeskim:mentions | umls-concept:C0599894 | lld:lifeskim |
| pubmed-article:21779463 | pubmed:issue | 6 | lld:pubmed |
| pubmed-article:21779463 | pubmed:dateCreated | 2011-7-22 | lld:pubmed |
| pubmed-article:21779463 | pubmed:abstractText | The MYC protein controls many cellular processes, including proliferation, cell cycle progression, cell growth, metabolism, angiogenesis, differentiation, cell adhesion, and motility. This is primarily achieved through transcriptional regulation of large gene networks that ultimately results in activation or repression of target genes. Given its broad regulatory scope, the expression of the MYC gene itself needs to be tightly controlled. Deregulation of MYC expression promotes tumorigenesis and, not surprisingly, MYC is frequently activated in many different human cancers. Furthermore, these tumors become highly dependent on sustained MYC expression, while MYC inactivation results in desirable anticancer effects, such as cell death, differentiation, and/or senescence. Thus, MYC has emerged as an attractive target for cancer therapy. In addition to regulating protein-coding genes, MYC also governs the expression of microRNAs, many of which have important regulatory roles in cancer development and progression. Here we will discuss how MYC-regulated miRNAs could be exploited for therapeutic development for cancer. | lld:pubmed |
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