Oncogenic activation of MYC proteins affects multiple intracellular pathways, culminating in neoplastic transformation in many cell types. MYC overexpression is involved in all aspects of tumor cell biology including proliferation, cell survival, differentiation, angiogenesis and metastasis. Furthermore, cell proliferation, metabolic boost and survival promoted by MYC produce cells with highly unstable genomes, contributing to tumor progression and maintenance. This study expands our knowledge about the impact of MYC oncogenes alterations on damage response and repair networks. Moreover, this study provides evidences that the histone demethylase LSD1 is a critical co-factor of MYCN repressive function in neuroblastoma and exerts a key role in the control of many important aspects of cell biology through the transcriptional regulation of specific target genes, suggesting that LSD1 inhibition may have strong therapeutic relevance to counteract MYCN-driven oncogenesis.

MYC proteins in human cancer: epigenetic changes and molecular targeting

2017

Abstract

Oncogenic activation of MYC proteins affects multiple intracellular pathways, culminating in neoplastic transformation in many cell types. MYC overexpression is involved in all aspects of tumor cell biology including proliferation, cell survival, differentiation, angiogenesis and metastasis. Furthermore, cell proliferation, metabolic boost and survival promoted by MYC produce cells with highly unstable genomes, contributing to tumor progression and maintenance. This study expands our knowledge about the impact of MYC oncogenes alterations on damage response and repair networks. Moreover, this study provides evidences that the histone demethylase LSD1 is a critical co-factor of MYCN repressive function in neuroblastoma and exerts a key role in the control of many important aspects of cell biology through the transcriptional regulation of specific target genes, suggesting that LSD1 inhibition may have strong therapeutic relevance to counteract MYCN-driven oncogenesis.
2017
it
File in questo prodotto:
File Dimensione Formato  
AMBROSIO.pdf

accesso solo da BNCF e BNCR

Tipologia: Altro materiale allegato
Licenza: Tutti i diritti riservati
Dimensione 13.02 MB
Formato Adobe PDF
13.02 MB Adobe PDF

I documenti in UNITESI sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/20.500.14242/322177
Il codice NBN di questa tesi è URN:NBN:IT:BNCF-322177