A5015680218- Cancer-related gene regulation
- Epigenetics and DNA Methylation
- Histone Deacetylase Inhibitors Research
- HER2/EGFR in Cancer Research
- Developmental Biology and Gene Regulation
- Hedgehog Signaling Pathway Studies
- Acute Lymphoblastic Leukemia research
- T-cell and Retrovirus Studies
- Genomics, phytochemicals, and oxidative stress
- RNA Interference and Gene Delivery
- Genetic and rare skin diseases.
- Microtubule and mitosis dynamics
- MicroRNA in disease regulation
- Cancer-related Molecular Pathways
- Immune Cell Function and Interaction
- Mitochondrial Function and Pathology
- Ubiquitin and proteasome pathways
- Cytokine Signaling Pathways and Interactions
- Synthesis of Organic Compounds
- Virus-based gene therapy research
- Circular RNAs in diseases
- Genomics and Chromatin Dynamics
- Cancer and Skin Lesions
- Genetic factors in colorectal cancer
- TGF-β signaling in diseases
Sapienza University of Rome
2011-2024
Italian Institute of Technology
2013-2021
University of L'Aquila
2004-2007
Istituto Pasteur
2005
Istituto Neurologico Mediterraneo
2005
Deregulated Notch signaling is associated with T-cell Acute Lymphoblastic Leukemia (T-ALL) development and progression. Increasing evidence reveals that pathway has an important role in the invasion ability of tumor cells, including leukemia, although underlying molecular mechanisms remain mostly unclear. Here, we show Notch3 a novel target protein prolyl-isomerase Pin1, which able to regulate processing stabilize cleaved product, leading increased expression intracellular domain (N3IC),...
Deregulated Notch signaling has been extensively linked to T-cell acute lymphoblastic leukemia (T-ALL). Here, we show a direct relationship between Notch3 receptor and Jagged1 ligand in human cell lines mouse model of T-ALL. We provide evidence that Notch-specific is new target gene. This essential event justifies an aberrant Notch3/Jagged1 cis-expression inside the same cell. Moreover, demonstrate Notch3-IC-overexpressing T lymphoma cells undergoes raft-associated constitutive processing....
Abstract Notch signaling is considered a rational target in the therapy of several cancers, particularly those harbouring gain function mutations, including T-cell acute lymphoblastic leukemia (T-ALL). Although currently available Notch-blocking agents are showing anti-tumor activity preclinical studies, they not effective all patients and often cause severe side-effects, limiting their widespread therapeutic use. Here, by functional biological analysis most representative molecules an house...
Notch dysregulation has been implicated in numerous tumors, including triple-negative breast cancer (TNBC), which is the subtype with worst clinical outcome. However, importance of individual receptors TNBC and their specific mechanism action remain to be elucidated, even if recent findings suggested a role activated-Notch3 subset TNBCs. Epidermal growth factor receptor (EGFR) overexpressed TNBCs but use anti-EGFR agents (including tyrosine kinase inhibitors, TKIs) not approved for treatment...
Colorectal cancer is characterized by well-known genetic defects and approximately 50% of cases harbor oncogenic Ras mutations. Increased expression Notch ligand Jagged1 occurs in several human malignancies, including colorectal cancer, correlates with progression, poor prognosis, recurrence. Herein, we demonstrated that was constitutively processed tumors mutant Kras, which ultimately triggered intrinsic reverse signaling via its nuclear-targeted intracellular domain Jag1-ICD. This process...
Abstract Sonic hedgehog (Shh) signaling is essential for proliferation of cerebellar granule cell progenitors (GCPs) and its misregulation linked to various disorders, including cancer medulloblastoma. The effects Shh pathway are mediated by the Gli family transcription factors, which controls expression a number target genes, Gli1 . Here, we identify Mastermind-like 1 (Maml1) as novel regulator since it interacts with proteins, working potent transcriptional coactivator. Notably, Maml1...
Notch signaling plays a complex role in carcinogenesis, and its pathway has both tumor-suppressor oncogenic components. In this study we investigated the effects of reactive oxygen species (ROS) on Notch1 outcome keratinocyte biology. We demonstrate that function contributes to arsenic-induced transformation. found acute exposure arsenite increases oxidative stress inhibits proliferation cells by upregulation p21(waf1/Cip1). The necessity p21(waf1/Cip1) for arsenite-induced cell death was...
Aberrant upregulation of NOTCH3 gene plays a critical role in cancer pathogenesis. However, the underlying mechanisms are still unknown. We tested here hypothesis that aberrant epigenetic modifications promoter region might account for its cells. compared DNA and histone methylation status human normal blood cells T cell acute lymphoblastic leukemia (T-ALL) lines, differentially expressing NOTCH3. found methylation, rather than hypomethylation, contributes towards establishing an active...
T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive blood cancer caused by the deregulation of key developmental pathways, including Notch signaling. Aberrant signaling in T-ALL occurs NOTCH1 gain-of-function mutations and NOTCH3 overexpression. Although assumed as a Notch1 target, machinery driving its transcription undefined subsets lacking activation. Here, we found that binding intracellular Notch3 domain, well activated fragment, to gene locus led recruitment H3K27 modifiers...
Abstract Mutation of the Golgi Ca 2+ -ATPase ATP2C1 is associated with deregulated calcium homeostasis and altered skin function. mutations have been identified as having a causative role in Hailey-Hailey disease, an autosomal-dominant disorder. Here, we crucial regulator epidermal through regulation oxidative stress. Upon inactivation, stress Notch1 activation were increased cultured human keratinocytes. Using RNA-seq experiments, found that DNA damage response (DDR) was consistently...