Ricerc@Sapienza

Glioblastomas (GBM) are the most aggressive form of primary brain tumors in humans.
A key feature of malignant gliomas is their cellular heterogeneity. In particular, the presence of
an undierentiated cell population of defined Glioblastoma Stem cells (GSCs) was reported. Increased
expression of anti-apoptotic and chemo-resistance genes in GCSs subpopulation favors their high
resistance to a broad spectrum of drugs. Our previous studies showed the ability of M2 muscarinic

Exposure of the developing or adult brain to ionizing radiation (IR) can cause cognitive impairment and/
or brain cancer, by targeting neural stem/progenitor cells (NSPCs). IR effects on NSPCs include transient
cell cycle arrest, permanent cell cycle exit/differentiation, or cell death, depending on the experimental
conditions. In vivo studies suggest that brain age influences NSPC response to IR, but whether this is
due to intrinsic NSPC changes or to niche environment modifications remains unclear. Here, we describe

Mutations in CDCA7, the SNF2 family protein HELLS (LSH), or the DNA methyltransferase DNMT3b cause immunodeficiency–centro-meric instability–facial anomalies (ICF) syndrome. While it has been speculated that DNA methylation defects cause this disease, little is known about the molecular function of CDCA7 and its functional relationship to HELLS and DNMT3b.

Cytoplasmic long non-coding RNAs have been shown to act at many different levels to control post-transcriptional gene expression, although their role in translational control is poorly understood. Here, we show that lnc-31, a non-coding RNA required for myoblast proliferation, promotes ROCK1 protein synthesis by stabilizing its translational activator, YB-1. We find that lnc-31 binds to the Rock1 mRNA as well as to the YB-1 protein and that translational activation requires physical interaction between the two RNA species.

This study aims to determine the interaction (uptake and biological effects on cell viability and cell cycle progression) of glucose capped silver nanoparticles (AgNPs-G) on human epithelioid cervix carcinoma (HeLa) cells, in relation to amount, 2 x 10(3) or 2 x 10(4) NPs/cell, and exposure time, up to 48 h.

Sirtuins, a family of nicotinamide adenine dinucleotide (NAD+)-dependent lysine deacetylases, are promising targets for anticancer treatment. Recently, we characterized a novel pan-sirtuin (SIRT) inhibitor, MC2494, displaying antiproliferative effects and able to induce death pathways in several human cancer cell lines and decrease tumor growth in vivo.

Notch signaling plays a complex role in carcinogenesis, and its signaling pathway has both tumor suppressor and oncogenic components. To identify regulators that might control this dual activity of NOTCH1, we screened a chemical library targeting kinases and identified Polo-like kinase 1 (PLK1) as one of the kinases involved in arsenite-induced NOTCH1 down-modulation. As PLK1 activity drives mitotic entry but also is inhibited after DNA damage, we investigated the PLK1-NOTCH1 interplay in the G2 phase of the cell cycle and in response to DNA damage.