Jun: A transcription factor becomes oncogenic
نویسندگان
چکیده
منابع مشابه
Proto-oncogenic miR-744 is upregulated by transcription factor c-Jun via a promoter activation mechanism
Upregulation of miR-744 is associated with poor prognosis in many types of cancer patients, but it is still unclear how miR-744 becomes elevated in these tumors. In this study, we found that ectopic c-Jun elevated miR-744 expression, whereas c-Jun attenuation reduced miR-744 expression. Chromatin immunoprecipitation assay confirmed the direct binding of c-Jun to the promoter of miR-744. The bin...
متن کاملJAC, a direct target of oncogenic transcription factor Jun, is involved in cell transformation and tumorigenesis.
Using subtractive hybridization techniques, we have isolated a gene termed JAC that is strongly and specifically activated in avian fibroblasts transformed by the v-jun oncogene of avian sarcoma virus 17 (ASV17), but not in cells transformed by other oncogenic agents. Furthermore, JAC is highly expressed in cell lines derived from jun-induced avian fibrosarcomas. Kinetic analysis using a doxycy...
متن کاملThe oncogenic transcription factor c-Jun regulates glutaminase expression and sensitizes cells to glutaminase-targeted therapy.
Many transformed cells exhibit altered glucose metabolism and increased utilization of glutamine for anabolic and bioenergetic processes. These metabolic adaptations, which accompany tumorigenesis, are driven by oncogenic signals. Here we report that the transcription factor c-Jun, product of the proto-oncogene JUN, is a key regulator of mitochondrial glutaminase (GLS) levels. Activation of c-J...
متن کاملHeparin-binding epidermal growth factor-like growth factor, a v-Jun target gene, induces oncogenic transformation.
Jun is a transcription factor belonging to the activator protein 1 family. A mutated version of Jun (v-Jun) transduced by the avian retrovirus ASV17 induces oncogenic transformation in avian cell cultures and sarcomas in young galliform birds. The oncogenicity of Jun probably results from transcriptional deregulation of v-Jun-responsive target genes. Here we describe the identification and char...
متن کاملTranscription factor c-Jun activation represses mdr-1 gene expression.
Expression of mdr-1 is complex and highly regulated. Several lines of evidence indirectly suggest that transcription factor c-Jun may negatively regulate human mdr-1 gene expression. We recently found that salvicine, a novel topoisomerase II inhibitor, is cytotoxic for multidrug resistance (MDR) tumor cells and down-regulates mdr-1 expression in MDR K562/A02 cells. Salvicine also stimulates a s...
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ژورنال
عنوان ژورنال: Cancer
سال: 1992
ISSN: 0008-543X
DOI: 10.1002/1097-0142(19920515)69:10<2610::aid-cncr2820691035>3.0.co;2-j