A5040275242- Cancer, Lipids, and Metabolism
- Diet and metabolism studies
- Cancer, Hypoxia, and Metabolism
- RNA Research and Splicing
- RNA modifications and cancer
- RNA and protein synthesis mechanisms
- Cancer-related molecular mechanisms research
- Cell Adhesion Molecules Research
- RNA Interference and Gene Delivery
- Metabolomics and Mass Spectrometry Studies
- Cancer-related gene regulation
- ATP Synthase and ATPases Research
- Melanoma and MAPK Pathways
- Molecular Biology Techniques and Applications
- Neurogenetic and Muscular Disorders Research
- Muscle Physiology and Disorders
- RNA regulation and disease
- Prenatal Screening and Diagnostics
- Craniofacial Disorders and Treatments
- Endoplasmic Reticulum Stress and Disease
- Congenital heart defects research
- Protein Kinase Regulation and GTPase Signaling
- Viral Infections and Immunology Research
- Heat shock proteins research
- Cardiomyopathy and Myosin Studies
National Research Council
2013-2024
Istituto di Genetica Molecolare
2013-2023
Gwangju Institute of Science and Technology
2021
International Centre for Genetic Engineering and Biotechnology
2013
Institute of Neurobiology and Molecular Medicine
2007
University of Pavia
1998
In heat-shocked human cells, heat shock factor 1 activates transcription of tandem arrays repetitive Satellite III (SatIII) DNA in pericentromeric heterochromatin. RNAs remain associated with sites nuclear stress bodies (nSBs). Here we use real-time RT-PCR to study the expression these genomic regions. Transcription is highly asymmetrical and most transcripts contain G-rich strand repeat. A low level detectable unstressed cells a 10(4)-fold induction occurs after shock. are induced by wide...
Alternative splicing is a key molecular mechanism for increasing the functional diversity of eukaryotic proteomes. A large body experimental data implicates aberrant in various human diseases, including cancer. Both mutations cis-acting elements and alterations expression and/or activity regulatory factors drastically affect profile many cancer-associated genes. In addition, several genes altered particular types cancer arguing direct role specific isoforms tumor progression. Deciphering...
Epithelial-to-mesenchymal transition (EMT) and its reversal (MET) are crucial cell plasticity programs that act during development tumor metastasis. We have previously shown the splicing factor proto-oncogene SF2/ASF impacts EMT/MET through production of a constitutively active splice variant Ron proto-oncogene. Using an in vitro model, we now show is also regulated by alternative associated with nonsense-mediated mRNA decay pathway (AS-NMD). Overexpression small interfering RNA experiments...
Epithelial-to-mesenchymal transition (EMT) is an embryonic program used by cancer cells to acquire invasive capabilities becoming metastatic. ΔRon, a constitutively active isoform of the Ron tyrosine kinase receptor, arises from skipping exon 11 and provided first example alternative splicing variant causatively linked activation tumor EMT. Splicing controlled two adjacent regulatory elements, silencer enhancer located in 12. The factor oncoprotein SRSF1 directly binds enhancer, induces...
Abstract Cancer cells exhibit metabolic plasticity to meet oncogene-driven dependencies while coping with nutrient availability. A better understanding of how systemic metabolism impacts the accumulation metabolites that reprogram tumor microenvironment (TME) and drive cancer could facilitate development precision nutrition approaches. Using Hi-MYC prostate mouse model, we demonstrated an obesogenic high-fat diet (HFD) rich in saturated fats accelerates c-MYC–driven invasive through...
Abstract Vascular lumen formation is a fundamental step during angiogenesis; yet, the molecular mechanisms underlying this process are poorly understood. Recent studies have shown that neural and vascular systems share common anatomical, functional similarities. Here we show organization of endothelial controlled at post-transcriptional level by alternative splicing (AS) regulator Nova2, which was previously considered to be cell-specific. Nova2 expressed angiogenesis its depletion disrupts...
The biological players involved in angiogenesis are only partially defined. Here, we report that endothelial cells (ECs) express a novel isoform of the cell-surface adhesion molecule L1CAM, termed L1-ΔTM. splicing factor NOVA2, which binds directly to L1CAM pre-mRNA, is necessary and sufficient for skipping transmembrane domain ECs, leading release soluble latter exerts high angiogenic function through both autocrine paracrine activities. Mechanistically, L1-ΔTM-induced requires fibroblast...
Alternative splicing is a key molecular mechanism for increasing the complexity of human transcriptome. Nearly all genes are regulated by alternative and deregulation this process has causative role in various diseases, including cancer. The discovery that alternatively spliced isoforms several expressed selectively tumor cells opened exciting possibility pharmacological treatment aberrant could lead to new anti-cancer therapeutic approaches. An isoform scatter factor receptor...
Abstract The Netrin-1 receptor UNC5B is an axon guidance regulator that also expressed in endothelial cells (ECs), where it finely controls developmental and tumor angiogenesis. In the absence of Netrin-1, induces apoptosis blocked upon binding. Here, we identify splicing isoform (called UNC5B-Δ8) exclusively by ECs generated through exon skipping NOVA2, alternative factor regulating vascular development. We show UNC5B-Δ8 a constitutively pro-apoptotic insensitive to required for specific...
Splicing of mouse immunoglobulin (IgM) exons M1 and M2 is directed by two juxtaposed regulatory elements, an enhancer inhibitor, located within the exon. A primary function to counteract allowing splicing occur. Here we show that inhibitor contains binding sites for polypyrimidine tract protein (PTB). Mutational analysis indicates only one these necessary sufficient direct inhibition both in vitro vivo. We demonstrate difference activity explained proximity intron. further presence results...