FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W110418765> ?p ?o ?g. }

• W110418765 abstract "The Myc oncoproteins belong to a family of transcription factors composed by Myc, N-Myc and L-Myc. The most studied components of this family are Myc and N-Myc because their expressions are frequently deregulated in a wide range of cancers. These oncoproteins can act both as activators or repressors of gene transcription. As activators, they heterodimerize with Max (Myc associated X-factor) and the heterodimer recognizes and binds a specific sequence elements (E-Box) onto gene promoters recruiting histone acetylase and inducing transcriptional activation. Myc-mediated transcriptional repression is a quite debated issue. One of the first mechanisms defined for the Myc-mediated transcriptional repression consisted in the interaction of Myc-Max complex Sp1 and/or Miz1 transcription factors already bound to gene promoters. This interaction may interfere with their activation functions by recruiting co-repressors such as Dnmt3 or HDACs. Moreover, in the absence of , Myc may interfere with the Sp1 activation function by direct interaction and subsequent recruitment of HDACs. More recently the Myc/Max complex was also shown to mediate transcriptional repression by direct binding to peculiar E-box.In this study we analyzed the role of Myc overexpression in Osteosarcoma and Neuroblastoma oncogenesis and the mechanisms underling to Myc function.Myc overexpression is known to correlate with chemoresistance in Osteosarcoma cells. We extended this study by demonstrating that c-Myc induces transcription of a panel of ABC drug transporter genes. ABCs are a large family trans-membrane transporter deeply involved in multi drug resistance. Furthermore expression levels of Myc, ABCC1, ABCC4 and ABCF1 were proved to be important prognostic tool to predict conventional therapy failure.N-Myc amplification/overexpression is the most important prognostic factor for Neuroblastoma. Cyclin G2 and Clusterin are two genes often down regulated in neuroblastoma cells. Cyclin G2 is an atypical member of Cyclin family and its expression is associated with terminal differentiation and apoptosis. Moreover it blocks cell cycle progression and induces cell growth arrest. Instead, CLU is a multifunctional protein involved in many physiological and pathological processes. Several lines of evidences support the view that CLU may act as a tumour suppressor in Neuroblastoma. In this thesis I showed that N-Myc represses CCNG2 and CLU transcription by different mechanisms. •N-Myc represses CCNG2 transcription by directly interacting with Sp1 bound in CCNG2 promoter and recruiting HDAC2. Importantly, reactivation of CCNG2 expression through epigenetic drugs partially reduces N-Myc and HDAC2 mediated cell proliferation.•N-Myc/Max complex represses CLU expression by direct binding to a peculiar E-box element on CLU promoter and by recruitment of HDACs and Polycomb Complexes, to the CLU promoter.Overall our findings strongly support the model in which Myc overexpression/amplification may contribute to some aspects of oncogenesis by a dual action: i) transcription activation of genes that confer a multidrug resistant phenotype to cancer cells; ii), transcription repression of genes involved in cell cycle inhibition and cellular differentiation." @default.
• W110418765 created "2016-06-24" @default.
• W110418765 creator A5025704120 @default.
• W110418765 date "2010-04-20" @default.
• W110418765 modified "2023-09-27" @default.
• W110418765 title "Myc-mediated control of gene transcription in cancer cells" @default.
• W110418765 cites W1480318984 @default.
• W110418765 cites W1494949608 @default.
• W110418765 cites W1520454142 @default.
• W110418765 cites W1543093074 @default.
• W110418765 cites W1548013608 @default.
• W110418765 cites W1583251544 @default.
• W110418765 cites W1595867557 @default.
• W110418765 cites W1599757231 @default.
• W110418765 cites W173611128 @default.
• W110418765 cites W1802071582 @default.
• W110418765 cites W1887854518 @default.
• W110418765 cites W1909200755 @default.
• W110418765 cites W1911655428 @default.
• W110418765 cites W1937649092 @default.
• W110418765 cites W1938893963 @default.
• W110418765 cites W1942629554 @default.
• W110418765 cites W1942778846 @default.
• W110418765 cites W1959907212 @default.
• W110418765 cites W1963633345 @default.
• W110418765 cites W1964742508 @default.
• W110418765 cites W1965948654 @default.
• W110418765 cites W1967596423 @default.
• W110418765 cites W1969321512 @default.
• W110418765 cites W1970233304 @default.
• W110418765 cites W1971209629 @default.
• W110418765 cites W1971658611 @default.
• W110418765 cites W1972778166 @default.
• W110418765 cites W1973759523 @default.
• W110418765 cites W1976229755 @default.
• W110418765 cites W1977479343 @default.
• W110418765 cites W1978440762 @default.
• W110418765 cites W1978735852 @default.
• W110418765 cites W1980110416 @default.
• W110418765 cites W1981904789 @default.
• W110418765 cites W1986962731 @default.
• W110418765 cites W1987599413 @default.
• W110418765 cites W1988622703 @default.
• W110418765 cites W1993522288 @default.
• W110418765 cites W1993969571 @default.
• W110418765 cites W1996940747 @default.
• W110418765 cites W1997614722 @default.
• W110418765 cites W1999424147 @default.
• W110418765 cites W2001793259 @default.
• W110418765 cites W2003026261 @default.
• W110418765 cites W2006036404 @default.
• W110418765 cites W2010031978 @default.
• W110418765 cites W2010697949 @default.
• W110418765 cites W2010982295 @default.
• W110418765 cites W2011795445 @default.
• W110418765 cites W2012398556 @default.
• W110418765 cites W2013121814 @default.
• W110418765 cites W2013205740 @default.
• W110418765 cites W2013729196 @default.
• W110418765 cites W2013851619 @default.
• W110418765 cites W2015085861 @default.
• W110418765 cites W2016646710 @default.
• W110418765 cites W2017438799 @default.
• W110418765 cites W2017761226 @default.
• W110418765 cites W2019903573 @default.
• W110418765 cites W2024280594 @default.
• W110418765 cites W2027558915 @default.
• W110418765 cites W2028859420 @default.
• W110418765 cites W2029172019 @default.
• W110418765 cites W2031719598 @default.
• W110418765 cites W2032972450 @default.
• W110418765 cites W2034176492 @default.
• W110418765 cites W2035648934 @default.
• W110418765 cites W2042752142 @default.
• W110418765 cites W2042777921 @default.
• W110418765 cites W2043848225 @default.
• W110418765 cites W2044033792 @default.
• W110418765 cites W2047816695 @default.
• W110418765 cites W2048768497 @default.
• W110418765 cites W2049119567 @default.
• W110418765 cites W2050249744 @default.
• W110418765 cites W2050358666 @default.
• W110418765 cites W2050767064 @default.
• W110418765 cites W2053706948 @default.
• W110418765 cites W2054193017 @default.
• W110418765 cites W2056772956 @default.
• W110418765 cites W2057654378 @default.
• W110418765 cites W2059627145 @default.
• W110418765 cites W2059880768 @default.
• W110418765 cites W2062290101 @default.
• W110418765 cites W2064735501 @default.
• W110418765 cites W2066246322 @default.
• W110418765 cites W2066663722 @default.
• W110418765 cites W2067606868 @default.
• W110418765 cites W2069795464 @default.
• W110418765 cites W2070672809 @default.
• W110418765 cites W2071368489 @default.
• W110418765 cites W2071491707 @default.
• W110418765 cites W2073101093 @default.
• W110418765 cites W2073159328 @default.

• next