<i>SNHG5</i> promotes colorectal cancer cell survival by counteracting STAU1-mediated mRNA destabilization

We currently have limited knowledge of the involvement of long non-coding RNAs (lncRNAs) in normal cellular processes and pathologies. Here, we identify and characterize SNHG5 as a stable cytoplasmic lncRNA with up-regulated expression in colorectal cancer. Depletion of SNHG5 induces cell cycle arrest and apoptosis in vitro and limits tumour outgrowth in vivo, whereas SNHG5 overexpression counteracts oxaliplatin-induced apoptosis. Using an unbiased approach, we identify 121 transcript sites interacting with SNHG5 in the cytoplasm. Importantly, knockdown of key SNHG5 target transcripts, including SPATS2, induces apoptosis and thus mimics the effect seen following SNHG5 depletion. Mechanistically, we suggest that SNHG5 stabilizes the target transcripts by blocking their degradation by STAU1. Accordingly, depletion of STAU1 rescues the apoptosis induced after SNHG5 knockdown. Hence, we characterize SNHG5 as a lncRNA promoting tumour cell survival in colorectal cancer and delineate a novel mechanism in which a cytoplasmic lncRNA functions through blocking the action of STAU1

Augmented Reality per Cultural Heritage: un prototipo per le tombe di Koguryo

Seguendo l'onda del successo delle applicazioni di augmented reality si è pensato di realizzare un'applicazione web-based che sfrutta le tecnologie di realtà aumentata per favorire la valorizzazione di un sito archeologico patrimonio dell'UNESCO; ovvero le tombe del sito archeologico di Koguryo. La tesi è stata svolta in collaborazione con il Corso di Laurea Magistrale in Science for Conservation and Restoration of Cultural Heritage (dell’Ateneo di Bologna). Per poter procedere alla realizzazione del progetto ci si è posti tre obiettivi principali: • permettere a chi utilizza l’applicazione di poter immergersi in una ‘visita virtuale’ facendo sì che l’utente possa sentirsi trasportato direttamente in loco. • fornire tutte le informazioni necessarie per la miglior comprensione di ciò che si ha davanti e per fare questo si è cercato il metodo più diretto ed accattivante in modo che tali nozioni possano essere adatte a tutte le tipologie di visitatori che un ipotetico sito archeologico potrebbe ospitare. • come ultimo punto è stato fondamentale fornire il progetto finito di un web hosting in modo da renderlo accessibile sia da mobile che da desktop in qualsiasi momento e in qualsiasi luogo si voglia far partire questa esperienza. La realizzazione di questo prototipo è stata pensata come una sorta di apripista per il perfezionamento e innovamento di quest'ultimo integrando tutte le tecnologie più recenti e all'avanguardia della realtà aumentata

The lncRNA MIR31HG regulates p16 INK4A expression to modulate senescence

Oncogene-induced senescence (OIS) can occur in response to oncogenic insults and is considered an important tumour suppressor mechanism. Here we identify the lncRNA MIR31HG as upregulated in OIS and find that knockdown of MIR31HG promotes a strong p16INK4A -dependent senescence phenotype. Under normal conditions, MIR31HG is found in both nucleus and cytoplasm, but following B-RAF expression MIR31HG is located mainly in the cytoplasm. We show that MIR31HG interacts with both INK4A and MIR31HG genomic regions and with Polycomb group (PcG) proteins, and that MIR31HG is required for PcG-mediated repression of the INK4A locus. We further identify a functional enhancer, located between MIR31HG and INK4A, which becomes activated during OIS and interacts with the MIR31HG promoter. Data from melanoma patients show a negative correlation between MIR31HG and p16INK4A expression levels, suggesting a role for this transcript in cancer. Hence, our data provide a new lncRNA-mediated regulatory mechanism for the tumour suppressor p16INK4A

The lncRNA MIR31HG regulates p16 INK4A expression to modulate senescence

Oncogene-induced senescence (OIS) can occur in response to oncogenic insults and is considered an important tumour suppressor mechanism. Here we identify the lncRNA MIR31HG as upregulated in OIS and find that knockdown of MIR31HG promotes a strong p16INK4A -dependent senescence phenotype. Under normal conditions, MIR31HG is found in both nucleus and cytoplasm, but following B-RAF expression MIR31HG is located mainly in the cytoplasm. We show that MIR31HG interacts with both INK4A and MIR31HG genomic regions and with Polycomb group (PcG) proteins, and that MIR31HG is required for PcG-mediated repression of the INK4A locus. We further identify a functional enhancer, located between MIR31HG and INK4A, which becomes activated during OIS and interacts with the MIR31HG promoter. Data from melanoma patients show a negative correlation between MIR31HG and p16INK4A expression levels, suggesting a role for this transcript in cancer. Hence, our data provide a new lncRNA-mediated regulatory mechanism for the tumour suppressor p16INK4A