VEROMIRNA

miR-483-3p and drug resistance in Hepatocarcinoma

 Coordinatore UNIVERSITA DEGLI STUDI GABRIELE D'ANNUNZIO DI CHIETI-PESCARA 

 Organization address address: Via dei Vestini 31
city: CHIETI
postcode: 66013

contact info
Titolo: Ms.
Nome: Elvira
Cognome: D' Annunzio
Email: send email
Telefono: 3908710000000

 Nazionalità Coordinatore Italy [IT]
 Totale costo 100˙000 €
 EC contributo 100˙000 €
 Programma FP7-PEOPLE
Specific programme "People" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
 Code Call FP7-PEOPLE-2011-CIG
 Funding Scheme MC-CIG
 Anno di inizio 2012
 Periodo (anno-mese-giorno) 2012-10-01   -   2016-09-30

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    UNIVERSITA DEGLI STUDI GABRIELE D'ANNUNZIO DI CHIETI-PESCARA

 Organization address address: Via dei Vestini 31
city: CHIETI
postcode: 66013

contact info
Titolo: Ms.
Nome: Elvira
Cognome: D' Annunzio
Email: send email
Telefono: 3908710000000

IT (CHIETI) coordinator 100˙000.00

Mappa


 Word cloud

Esplora la "nuvola delle parole (Word Cloud) per avere un'idea di massima del progetto.

agent    de    cells    expression    drug    shown    hepg       azacytidine    resistance    hep    induced    mir    regulated    lines       treatment    regulation    found    induces    apoptosis    igf    locus    gene    chemotherapeutic    hcc    fu    methylating    cell   

 Obiettivo del progetto (Objective)

'Hsa-mir-483 is located within intron 2 of the INS-IGF2 gene. We have previously shown oncogenic features of miR-483-3p targeting the pro-apoptotic gene BBC3/PUMA (P53 up-regulated modulator of apoptosis gene) giving drug resistance to cells. Generally the IGF2 and miR-483 expression are strictly correlated although we have demonstrated that expression of miR-483 can be induced independently of IGF2 by the oncoprotein b-catenin. In Hepatocarcinoma (HCC) IGF2/483 locus is often over-expressed probably by Loss of Imprinting (LOI) at the IGF2/H19 imprinted control region (ICR) and HepG2 and Hep3B HCC cell lines shown the entire IGF2/483 locus up-regulated. As a matter of fact we found that the treatment with the de-methylating agent 5-azacytidine, induces an important down-regulation of IGF2 and miR-483-3p genes. Moreover, during the course of our study we found that the chemotherapeutic drug 5-fluoruracyl (5-FU) induces increased expression of miR-483-3p in HepG2 and Hep3B cells. 5-FU treatment does not affect all the HCC cell lines that we tested suggesting a possible heterogeneity in cellular drug resistance dependently from miR-483-3p induced expression. Aim of this project is to investigate the mechanism involved in the 5-FU/miR-483 regulation, identify its importance in chemotherapeutic resistance in HCC primary tissues and explore if a concomitant treatment with the de-methylating agent 5-azacytidine and chemotherapeutic 5-FU, could improve the susceptibility to apoptosis of cancer cells.'

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