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TETCOLON SIGNED

Dissecting the role of the epigenetic regulator TET2 in colorectal cancer

Total Cost €

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EC-Contrib. €

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Partnership

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 TETCOLON project word cloud

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preliminary    genes    instability    contain    family    basic    5hmc    methylcytosine    ultimately    therapies    cancer    dna    causal    knockdown    deficient    molecular    tissue    active    crc    protein    methylome    bioinformatics    deficiency    suppression    helping    pathogenesis    elucidate    indicates    tet    mutational    clear    genetic    techniques    contributes    defects    mechanism    survival    load    cells    mouse    induces    disciplinary    revealed    tumor    epithelial    oxidized    epigenetics    dioxygenases    event    crcs    driver    expression    methylation    stability    epigenome    human    link    supporting    demethylation    5mcs    suggests    epigenetic    eleven    methylated    accumulation    aberrantly    biology    tet2    seq    3d    tet1    pathological    reprogramming    colorectal    translocation    combining    clinico    significance    rna    transcriptome    epi    mrna    predictive    perturbed    edge    virtually    genomic    ten    patterns    vulnerabilities    translational    predicts    mediated    oncogenic    cutting    correlations    oxidize    levels    epigenomic    cell    carcinogenesis    probe    colonic    5mc    therapeutic    normal    bystander    culture    innovative    biomarker    hydroxymethylcytosine   

Project "TETCOLON" data sheet

The following table provides information about the project.

Coordinator
UNIVERSITA DEGLI STUDI DI PAVIA 

Organization address
address: STRADA NUOVA 65
city: PAVIA
postcode: 27100
website: www.unipv.it

contact info
title: n.a.
name: n.a.
surname: n.a.
function: n.a.
email: n.a.
telephone: n.a.
fax: n.a.

 Coordinator Country Italy [IT]
 Total cost 183˙473 €
 EC max contribution 183˙473 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2019
 Funding Scheme MSCA-IF-EF-RI
 Starting year 2020
 Duration (year-month-day) from 2020-09-01   to  2022-08-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    UNIVERSITA DEGLI STUDI DI PAVIA IT (PAVIA) coordinator 183˙473.00

Map

 Project objective

Colorectal cancer (CRC) results from the accumulation of genetic and epigenetic changes in colonic epithelial cells. Epigenome studies revealed that virtually all CRCs contain aberrantly methylated genes and perturbed methylation patterns. Ten-Eleven Translocation (TET) protein family dioxygenases oxidize 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC) and further to other oxidized 5mCs, supporting active DNA demethylation and helping maintain epigenomic stability. Loss of TET1 is an oncogenic driver in some CRCs. My preliminary analysis indicates that human CRCs have low TET2 mRNA levels compared to normal colorectal tissue, and suggests that low TET2 expression predicts increased mutational load and reduced overall survival. However, whether TET2 deficiency contributes to CRC pathogenesis, or represents a bystander event, remains to be established. In this proposal, I will elucidate the role of TET2 in CRC pathogenesis by testing whether TET2 knockdown induces methylome and transcriptome reprogramming, ultimately promoting (epi)genomic instability and tumor growth. I will also investigate correlations between TET2 defects and molecular/clinico-pathological parameters, and probe TET2 expression as predictive biomarker of response to CRC therapies. With these aims, I will use a multi-disciplinary approach, combining cell biology, cancer epigenetics, bioinformatics, human and mouse studies with cutting-edge techniques such as 3D cell culture and RNA-seq. This study should establish a clear causal link between TET2 loss and CRC pathogenesis, providing new insight into the mechanism of TET2-mediated tumor suppression and leading to the development of innovative therapies that exploit vulnerabilities of TET2-deficient CRC cells. Overall, this project has both basic and translational significance, and the potential to advance our understanding of CRC carcinogenesis and therapeutic response.

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The information about "TETCOLON" are provided by the European Opendata Portal: CORDIS opendata.

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