The kinase inhibitor SI113 induces autophagy and synergizes with quinacrine in hindering the growth of human glioblastoma multiforme cells
Identifieur interne : 000342 ( Main/Exploration ); précédent : 000341; suivant : 000343The kinase inhibitor SI113 induces autophagy and synergizes with quinacrine in hindering the growth of human glioblastoma multiforme cells
Auteurs : Silvia Matteoni [Italie] ; Claudia Abbruzzese [Italie] ; Paola Matarrese [Italie] ; Gabriele De Luca [Italie] ; Anna M. Mileo [Italie] ; Stefania Miccadei [Italie] ; Silvia Schenone [Italie] ; Francesca Musumeci [Italie] ; Tobias L. Haas [Italie] ; Giovanni Sette [Italie] ; Carmine M. Carapella [Italie] ; Rosario Amato [Italie] ; Nicola Perrotti [Italie] ; Michele Signore [Italie] ; Marco G. Paggi [Italie]Source :
- Journal of Experimental & Clinical Cancer Research : CR [ 0392-9078 ] ; 2019.
Abstract
Glioblastoma multiforme (GBM), due to its location, aggressiveness, heterogeneity and infiltrative growth, is characterized by an exceptionally dismal clinical outcome. The small molecule SI113, recently identified as a SGK1 inhibitor, has proven to be effective in restraining GBM growth in vitro and in vivo, showing also encouraging results when employed in combination with other antineoplastic drugs or radiotherapy. Our aim was to explore the pharmacological features of SI113 in GBM cells in order to elucidate the pivotal molecular pathways affected by the drug. Such knowledge would be of invaluable help in conceiving a rational offensive toward GBM.
We employed GBM cell lines, either established or primary (neurospheres), and used a Reverse-Phase Protein Arrays (RPPA) platform to assess the effect of SI113 upon 114 protein factors whose post-translational modifications are associated with activation or repression of specific signal transduction cascades.
SI113 strongly affected the PI3K/mTOR pathway, evoking a pro-survival autophagic response in neurospheres. These results suggested the use of SI113 coupled, for maximum efficiency, with autophagy inhibitors. Indeed, the association of SI113 with an autophagy inhibitor, the antimalarial drug quinacrine, induced a strong synergistic effect in inhibiting GBM growth properties in all the cells tested, including neurospheres.
RPPA clearly identified the molecular pathways influenced by SI113 in GBM cells, highlighting their vulnerability when the drug was administered in association with autophagy inhibitors, providing a strong molecular rationale for testing SI113 in clinical trials in associative GBM therapy.
The online version of this article (10.1186/s13046-019-1212-1) contains supplementary material, which is available to authorized users.
Url:
DOI: 10.1186/s13046-019-1212-1
PubMed: 31101126
PubMed Central: 6525441
Affiliations:
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Le document en format XML
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">The kinase inhibitor SI113 induces autophagy and synergizes with quinacrine in hindering the growth of human glioblastoma multiforme cells</title>
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<institution>Department of “Scienze della Salute”,</institution>
<institution>University “Magna Graecia” of Catanzaro,</institution>
</institution-wrap>
Catanzaro, Italy</nlm:aff>
<country xml:lang="fr">Italie</country>
<wicri:regionArea>Catanzaro</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Perrotti, Nicola" sort="Perrotti, Nicola" uniqKey="Perrotti N" first="Nicola" last="Perrotti">Nicola Perrotti</name>
<affiliation wicri:level="1"><nlm:aff id="Aff9"><institution-wrap><institution-id institution-id-type="ISNI">0000 0001 2168 2547</institution-id>
<institution-id institution-id-type="GRID">grid.411489.1</institution-id>
<institution>Department of “Scienze della Salute”,</institution>
<institution>University “Magna Graecia” of Catanzaro,</institution>
</institution-wrap>
Catanzaro, Italy</nlm:aff>
<country xml:lang="fr">Italie</country>
<wicri:regionArea>Catanzaro</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Signore, Michele" sort="Signore, Michele" uniqKey="Signore M" first="Michele" last="Signore">Michele Signore</name>
<affiliation wicri:level="1"><nlm:aff id="Aff10"><institution-wrap><institution-id institution-id-type="ISNI">0000 0000 9120 6856</institution-id>
<institution-id institution-id-type="GRID">grid.416651.1</institution-id>
<institution>RPPA Unit, Proteomics Area, Core Facilities,</institution>
<institution>Istituto Superiore di Sanità,</institution>
</institution-wrap>
Viale Regina Elena 299, 00162 Rome, Italy</nlm:aff>
<country xml:lang="fr">Italie</country>
<wicri:regionArea>Viale Regina Elena 299, 00162 Rome</wicri:regionArea>
<placeName><settlement type="city">Rome</settlement>
<region nuts="2">Latium</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Paggi, Marco G" sort="Paggi, Marco G" uniqKey="Paggi M" first="Marco G." last="Paggi">Marco G. Paggi</name>
<affiliation wicri:level="1"><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="ISNI">0000 0004 1760 5276</institution-id>
<institution-id institution-id-type="GRID">grid.417520.5</institution-id>
<institution>Section of Cellular Networks and Molecular Therapeutic Targets, Proteomics Unit,</institution>
<institution>IRCCS - Regina Elena National Cancer Institute,</institution>
</institution-wrap>
Via Elio Chianesi 53, 00144 Rome, Italy</nlm:aff>
<country xml:lang="fr">Italie</country>
<wicri:regionArea>Via Elio Chianesi 53, 00144 Rome</wicri:regionArea>
<placeName><settlement type="city">Rome</settlement>
<region nuts="2">Latium</region>
</placeName>
</affiliation>
</author>
</analytic>
<series><title level="j">Journal of Experimental & Clinical Cancer Research : CR</title>
<idno type="ISSN">0392-9078</idno>
<idno type="eISSN">1756-9966</idno>
<imprint><date when="2019">2019</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc><textClass></textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en"><sec><title>Background</title>
<p id="Par1">Glioblastoma multiforme (GBM), due to its location, aggressiveness, heterogeneity and infiltrative growth, is characterized by an exceptionally dismal clinical outcome. The small molecule SI113, recently identified as a SGK1 inhibitor, has proven to be effective in restraining GBM growth in vitro and in vivo, showing also encouraging results when employed in combination with other antineoplastic drugs or radiotherapy. Our aim was to explore the pharmacological features of SI113 in GBM cells in order to elucidate the pivotal molecular pathways affected by the drug. Such knowledge would be of invaluable help in conceiving a rational offensive toward GBM.</p>
</sec>
<sec><title>Methods</title>
<p id="Par2">We employed GBM cell lines, either established or primary (neurospheres), and used a Reverse-Phase Protein Arrays (RPPA) platform to assess the effect of SI113 upon 114 protein factors whose post-translational modifications are associated with activation or repression of specific signal transduction cascades.</p>
</sec>
<sec><title>Results</title>
<p id="Par3">SI113 strongly affected the PI3K/mTOR pathway, evoking a pro-survival autophagic response in neurospheres. These results suggested the use of SI113 coupled, for maximum efficiency, with autophagy inhibitors. Indeed, the association of SI113 with an autophagy inhibitor, the antimalarial drug quinacrine, induced a strong synergistic effect in inhibiting GBM growth properties in all the cells tested, including neurospheres.</p>
</sec>
<sec><title>Conclusions</title>
<p id="Par4">RPPA clearly identified the molecular pathways influenced by SI113 in GBM cells, highlighting their vulnerability when the drug was administered in association with autophagy inhibitors, providing a strong molecular rationale for testing SI113 in clinical trials in associative GBM therapy.</p>
</sec>
<sec><title>Electronic supplementary material</title>
<p>The online version of this article (10.1186/s13046-019-1212-1) contains supplementary material, which is available to authorized users.</p>
</sec>
</div>
</front>
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</back>
</TEI>
<affiliations><list><country><li>Italie</li>
</country>
<region><li>Latium</li>
</region>
<settlement><li>Rome</li>
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</tree>
</affiliations>
</record>
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