SOX7 promotes the maintenance and proliferation of B cell precursor acute lymphoblastic cells
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Sara Cuvertino1,4, Genny Filiciotto1, Ashish Masurekar2, Vaskar Saha2,3, Georges Lacaud1, Valerie Kouskoff1
1Cancer Research UK Manchester Institute, The University of Manchester, Manchester M20 4BX, UK
2Children’s Cancer Group, Institute of Cancer Sciences, The University of Manchester, Manchester M20 4BX, UK
3TCS Translational Cancer Research Centre, Tata Medical Centre, Kolkata 700156, India
4Present address: Genetic Medicine, Institute of Human Development, University of Manchester, St Mary’s Hospital, Manchester M13 9WL, UK
Georges Lacaud, email: [email protected]
Valerie Kouskoff, email: [email protected]
Keywords: SOX7, leukemia, B-ALL
Received: February 19, 2016 Accepted: June 17, 2016 Published: July 7, 2016
B cell precursor acute lymphoblastic leukemia (BCP-ALL) is the most frequent type of cancer in children. Despite progresses in curative treatment, intensive chemotherapy regimens still cause life threatening complications. A better understanding of the molecular mechanisms underlying the emergence and maintenance of BCP-ALL is fundamental for the development of novel therapies. Here, we establish that SOX7 is frequently and specifically expressed in BCP-ALL and that the expression of this transcription factor does not correlate with any specific cytogenetic abnormalities. Using human leukemia model systems, we establish that the down-regulation of SOX7 in BCP-ALL causes a significant decrease in proliferation and clonogenicity in vitro that correlates with a delay in leukemia initiation and burden in vivo. Overall, these results identify a novel and important functional role for the transcription factor SOX7 in promoting the maintenance of BCP-ALL.
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