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            <title xml:lang="en">E2F1 inhibition mediates cell death of metastatic melanoma</title>
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                <forename type="first">Florian</forename>
                <surname>Rouaud</surname>
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                <forename type="first">Stéphane</forename>
                <surname>Rocchi</surname>
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            <funder>This research was supported by INSERM, University of Nice Sophia-Antipolis, INSERM transfert (COPOC grant), and ARC contract no. SFI 20121205378, by grants from « European Genomic Institute for Diabetes » (E.G.I.D, ANR-10-LABX-46 to J.-S.A.). M.C. is a recipient of a doctoral fellowship from the ARC. INSERM U1065, team 1 is « équipe labelisée ARC 2016».</funder>
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            <idno type="halRefHtml">&lt;i&gt;Cell Death and Disease&lt;/i&gt;, 2018, 9 (5), pp.527. &lt;a target="_blank" href="https://dx.doi.org/10.1038/s41419-018-0566-1"&gt;&amp;#x27E8;10.1038/s41419-018-0566-1&amp;#x27E9;&lt;/a&gt;</idno>
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            <idno type="stamp" n="INSERM">INSERM - Institut national de la santé et de la recherche médicale</idno>
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            <idno type="stamp" n="IRCAN">Institut de Recherche sur le Cancer et le Vieillissement </idno>
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                <title xml:lang="en">E2F1 inhibition mediates cell death of metastatic melanoma</title>
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                    <forename type="first">Stéphane</forename>
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                <title level="j">Cell Death and Disease</title>
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                  <publisher>Nature Publishing Group</publisher>
                  <biblScope unit="volume">9</biblScope>
                  <biblScope unit="issue">5</biblScope>
                  <biblScope unit="pp">527</biblScope>
                  <date type="datePub">2018-05</date>
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              <p>Melanoma is one of the most lethal cancers when it reaches a metastatic stage. Despite advancements in targeted therapies (BRAF inhibitors) or immunotherapies (anti-CTLA-4 or anti-PD1), most patients with melanoma will need additional treatment. Thus, there is an urgent need to develop new therapeutical approaches to bypass resistance and achieve more prolonged responses. In this context, we were interested in E2F1, a transcription factor that plays a major role in the control of cell cycle under physiological and pathological conditions. Here we confirmed that E2F1 is highly expressed in melanoma cells. Inhibition of E2F1 activity further increased melanoma cell death and senescence, both in vitro and in vivo. Moreover, blocking E2F1 also induced death of melanoma cells resistant to BRAF inhibitors. In conclusion, our studies suggest that targeting the E2F1 signaling pathway may be therapeutically relevant for melanoma.</p>
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