RETRACTED ARTICLE: Increased survival and cell cycle progression pathways are required for EWS/FLI1-induced malignant transformation
Ewing sarcoma (ES) is the second most frequent childhood bone cancer driven by the EWS/FLI1 (EF) fusion protein. Genetically defined ES models are needed to understand how EF expression changes bone precursor cell differentiation, how ES arises and through which mechanisms of inhibition it can be ta...
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| creator | Javaheri, Tahereh Kazemi, Zahra Pencik, Jan Pham, Ha TT Kauer, Maximilian Noorizadeh, Rahil Sax, Barbara Nivarthi, Harini Schlederer, Michaela Maurer, Barbara Hofbauer, Maximillian Aryee, Dave NT Wiedner, Marc Tomazou, Eleni M Logan, Malcolm Hartmann, Christine Tuckermann, Jan P Kenner, Lukas Mikula, Mario Dolznig, Helmut Üren, Aykut Richter, Günther H Grebien, Florian Kovar, Heinrich Moriggl, Richard |
| description | Ewing sarcoma (ES) is the second most frequent childhood bone cancer driven by the EWS/FLI1 (EF) fusion protein. Genetically defined ES models are needed to understand how EF expression changes bone precursor cell differentiation, how ES arises and through which mechanisms of inhibition it can be targeted. We used mesenchymal Prx1-directed conditional EF expression in mice to study bone development and to establish a reliable sarcoma model. EF expression arrested early chondrocyte and osteoblast differentiation due to changed signaling pathways such as hedgehog, WNT or growth factor signaling. Mesenchymal stem cells (MSCs) expressing EF showed high self-renewal capacity and maintained an undifferentiated state despite high apoptosis. Blocking apoptosis through enforced BCL2 family member expression in MSCs promoted efficient and rapid sarcoma formation when transplanted to immunocompromised mice. Mechanistically, high BCL2 family member and CDK4, but low P53 and INK4A protein expression synergized in Ewing-like sarcoma development. Functionally, knockdown of
Mcl1
or
Cdk4
or their combined pharmacologic inhibition resulted in growth arrest and apoptosis in both established human ES cell lines and EF-transformed mouse MSCs. Combinatorial targeting of survival and cell cycle progression pathways could counteract this aggressive childhood cancer. |
| doi_str_mv | 10.1038/cddis.2016.268 |
| format | Article |
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Mcl1
or
Cdk4
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Mcl1
or
Cdk4
or their combined pharmacologic inhibition resulted in growth arrest and apoptosis in both established human ES cell lines and EF-transformed mouse MSCs. Combinatorial targeting of survival and cell cycle progression pathways could counteract this aggressive childhood cancer.</description><subject>13/109</subject><subject>13/2</subject><subject>13/31</subject><subject>13/51</subject><subject>631/67/1344</subject><subject>631/67/1798</subject><subject>631/80/82/23</subject><subject>631/80/86</subject><subject>82/1</subject><subject>Antibodies</subject><subject>Biochemistry</subject><subject>Cell Biology</subject><subject>Cell Culture</subject><subject>Immunology</subject><subject>Life 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H</au><au>Grebien, Florian</au><au>Kovar, Heinrich</au><au>Moriggl, Richard</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>RETRACTED ARTICLE: Increased survival and cell cycle progression pathways are required for EWS/FLI1-induced malignant transformation</atitle><jtitle>Cell death & disease</jtitle><stitle>Cell Death Dis</stitle><date>2016-10-13</date><risdate>2016</risdate><volume>7</volume><issue>10</issue><spage>e2419</spage><epage>e2419</epage><pages>e2419-e2419</pages><issn>2041-4889</issn><eissn>2041-4889</eissn><abstract>Ewing sarcoma (ES) is the second most frequent childhood bone cancer driven by the EWS/FLI1 (EF) fusion protein. Genetically defined ES models are needed to understand how EF expression changes bone precursor cell differentiation, how ES arises and through which mechanisms of inhibition it can be targeted. We used mesenchymal Prx1-directed conditional EF expression in mice to study bone development and to establish a reliable sarcoma model. EF expression arrested early chondrocyte and osteoblast differentiation due to changed signaling pathways such as hedgehog, WNT or growth factor signaling. Mesenchymal stem cells (MSCs) expressing EF showed high self-renewal capacity and maintained an undifferentiated state despite high apoptosis. Blocking apoptosis through enforced BCL2 family member expression in MSCs promoted efficient and rapid sarcoma formation when transplanted to immunocompromised mice. Mechanistically, high BCL2 family member and CDK4, but low P53 and INK4A protein expression synergized in Ewing-like sarcoma development. Functionally, knockdown of
Mcl1
or
Cdk4
or their combined pharmacologic inhibition resulted in growth arrest and apoptosis in both established human ES cell lines and EF-transformed mouse MSCs. Combinatorial targeting of survival and cell cycle progression pathways could counteract this aggressive childhood cancer.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><doi>10.1038/cddis.2016.268</doi><oa>free_for_read</oa></addata></record> |
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| subjects | 13/109 13/2 13/31 13/51 631/67/1344 631/67/1798 631/80/82/23 631/80/86 82/1 Antibodies Biochemistry Cell Biology Cell Culture Immunology Life Sciences original-article |
| title | RETRACTED ARTICLE: Increased survival and cell cycle progression pathways are required for EWS/FLI1-induced malignant transformation |
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