RUNX2 regulates leukemic cell metabolism and chemotaxis in high-risk T cell acute lymphoblastic leukemia.

T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematologic malignancy with inferior outcome compared to B-cell ALL. Here, we showed that Runt-related transcription factor 2, RUNX2 was upregulated in high-risk T-ALL with KMT2A rearrangements (KMT2A-R) or an immature immunophenotype. In...

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Main Authors: Matthijssens, Filip, Sharma, Nitesh D, Nysus, Monique, Nickl, Christian K, Kang, Huining, Perez, Dominique R, Lintermans, Beatrice, Van Loocke, Wouter, Roels, Juliette, Peirs, Sofie, Demoen, Lisa, Pieters, Tim, Reunes, Lindy, Lammens, Tim, De Moerloose, Barbara, Van Nieuwerburgh, Filip, Deforce, Dieter L, Cheung, Laurence, Kotecha, Rishi, Risseeuw, Martijn DP, Van Calenbergh, Serge, Takarada, Takeshi, Yoneda, Yukio, van Delft, Frederik W, Lock, Richard B, Merkley, Seth D, Chigaev, Alexandre, Sklar, Larry A, Mullighan, Charles G, Loh, Mignon L, Winter, Stuart S, Hunger, Stephen P, Goossens, Steven, Castillo, Eliseo F, Ornatowski, Wojciech, Van Vlierberghe, Pieter, Matlawska-Wasowska, Ksenia
Format: Journal Article
Language:English
Published: 2021
Subjects:
Online Access:http://purl.org/au-research/grants/nhmrc/1142627
http://hdl.handle.net/20.500.11937/82712
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author Matthijssens, Filip
Sharma, Nitesh D
Nysus, Monique
Nickl, Christian K
Kang, Huining
Perez, Dominique R
Lintermans, Beatrice
Van Loocke, Wouter
Roels, Juliette
Peirs, Sofie
Demoen, Lisa
Pieters, Tim
Reunes, Lindy
Lammens, Tim
De Moerloose, Barbara
Van Nieuwerburgh, Filip
Deforce, Dieter L
Cheung, Laurence
Kotecha, Rishi
Risseeuw, Martijn DP
Van Calenbergh, Serge
Takarada, Takeshi
Yoneda, Yukio
van Delft, Frederik W
Lock, Richard B
Merkley, Seth D
Chigaev, Alexandre
Sklar, Larry A
Mullighan, Charles G
Loh, Mignon L
Winter, Stuart S
Hunger, Stephen P
Goossens, Steven
Castillo, Eliseo F
Ornatowski, Wojciech
Van Vlierberghe, Pieter
Matlawska-Wasowska, Ksenia
author_facet Matthijssens, Filip
Sharma, Nitesh D
Nysus, Monique
Nickl, Christian K
Kang, Huining
Perez, Dominique R
Lintermans, Beatrice
Van Loocke, Wouter
Roels, Juliette
Peirs, Sofie
Demoen, Lisa
Pieters, Tim
Reunes, Lindy
Lammens, Tim
De Moerloose, Barbara
Van Nieuwerburgh, Filip
Deforce, Dieter L
Cheung, Laurence
Kotecha, Rishi
Risseeuw, Martijn DP
Van Calenbergh, Serge
Takarada, Takeshi
Yoneda, Yukio
van Delft, Frederik W
Lock, Richard B
Merkley, Seth D
Chigaev, Alexandre
Sklar, Larry A
Mullighan, Charles G
Loh, Mignon L
Winter, Stuart S
Hunger, Stephen P
Goossens, Steven
Castillo, Eliseo F
Ornatowski, Wojciech
Van Vlierberghe, Pieter
Matlawska-Wasowska, Ksenia
author_sort Matthijssens, Filip
building Curtin Institutional Repository
collection Online Access
description T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematologic malignancy with inferior outcome compared to B-cell ALL. Here, we showed that Runt-related transcription factor 2, RUNX2 was upregulated in high-risk T-ALL with KMT2A rearrangements (KMT2A-R) or an immature immunophenotype. In KMT2A-R cells, we identified RUNX2 as a direct target of the KMT2A chimeras, where it reciprocally bound the KMT2A promoter, establishing a regulatory feed-forward mechanism. Notably, RUNX2 was required for survival of immature and KMT2A-R T-ALL cells in vitro and in vivo. We reported direct transcriptional regulation of CXCR4 signaling by RUNX2, thereby promoting chemotaxis, adhesion and homing to medullary and extramedullary sites. RUNX2 enabled these energy-demanding processes by increasing metabolic activity in T-ALL cells through positive regulation of both glycolysis and oxidative phosphorylation. Concurrently, RUNX2 upregulation increased mitochondrial dynamics and biogenesis in T-ALL cells. Finally, as a proof of concept, we demonstrated that immature and KMT2A-R T-ALL cells were vulnerable to pharmacological targeting of the interaction between RUNX2 and its co-factor CBFβ. In conclusion, we showed that RUNX2 acts as a dependency factor in high-risk subtypes of human T-ALL through concomitant regulation of tumour metabolism and leukemic cell migration.
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institution Curtin University Malaysia
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publishDate 2021
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spelling curtin-20.500.11937-827122021-03-18T03:53:24Z RUNX2 regulates leukemic cell metabolism and chemotaxis in high-risk T cell acute lymphoblastic leukemia. Matthijssens, Filip Sharma, Nitesh D Nysus, Monique Nickl, Christian K Kang, Huining Perez, Dominique R Lintermans, Beatrice Van Loocke, Wouter Roels, Juliette Peirs, Sofie Demoen, Lisa Pieters, Tim Reunes, Lindy Lammens, Tim De Moerloose, Barbara Van Nieuwerburgh, Filip Deforce, Dieter L Cheung, Laurence Kotecha, Rishi Risseeuw, Martijn DP Van Calenbergh, Serge Takarada, Takeshi Yoneda, Yukio van Delft, Frederik W Lock, Richard B Merkley, Seth D Chigaev, Alexandre Sklar, Larry A Mullighan, Charles G Loh, Mignon L Winter, Stuart S Hunger, Stephen P Goossens, Steven Castillo, Eliseo F Ornatowski, Wojciech Van Vlierberghe, Pieter Matlawska-Wasowska, Ksenia Cell migration/adhesion Leukemias Molecular biology Oncology T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematologic malignancy with inferior outcome compared to B-cell ALL. Here, we showed that Runt-related transcription factor 2, RUNX2 was upregulated in high-risk T-ALL with KMT2A rearrangements (KMT2A-R) or an immature immunophenotype. In KMT2A-R cells, we identified RUNX2 as a direct target of the KMT2A chimeras, where it reciprocally bound the KMT2A promoter, establishing a regulatory feed-forward mechanism. Notably, RUNX2 was required for survival of immature and KMT2A-R T-ALL cells in vitro and in vivo. We reported direct transcriptional regulation of CXCR4 signaling by RUNX2, thereby promoting chemotaxis, adhesion and homing to medullary and extramedullary sites. RUNX2 enabled these energy-demanding processes by increasing metabolic activity in T-ALL cells through positive regulation of both glycolysis and oxidative phosphorylation. Concurrently, RUNX2 upregulation increased mitochondrial dynamics and biogenesis in T-ALL cells. Finally, as a proof of concept, we demonstrated that immature and KMT2A-R T-ALL cells were vulnerable to pharmacological targeting of the interaction between RUNX2 and its co-factor CBFβ. In conclusion, we showed that RUNX2 acts as a dependency factor in high-risk subtypes of human T-ALL through concomitant regulation of tumour metabolism and leukemic cell migration. 2021 Journal Article http://hdl.handle.net/20.500.11937/82712 10.1172/JCI141566 eng http://purl.org/au-research/grants/nhmrc/1142627 http://purl.org/au-research/grants/nhmrc/1059804 http://purl.org/au-research/grants/nhmrc/1157871 fulltext
spellingShingle Cell migration/adhesion
Leukemias
Molecular biology
Oncology
Matthijssens, Filip
Sharma, Nitesh D
Nysus, Monique
Nickl, Christian K
Kang, Huining
Perez, Dominique R
Lintermans, Beatrice
Van Loocke, Wouter
Roels, Juliette
Peirs, Sofie
Demoen, Lisa
Pieters, Tim
Reunes, Lindy
Lammens, Tim
De Moerloose, Barbara
Van Nieuwerburgh, Filip
Deforce, Dieter L
Cheung, Laurence
Kotecha, Rishi
Risseeuw, Martijn DP
Van Calenbergh, Serge
Takarada, Takeshi
Yoneda, Yukio
van Delft, Frederik W
Lock, Richard B
Merkley, Seth D
Chigaev, Alexandre
Sklar, Larry A
Mullighan, Charles G
Loh, Mignon L
Winter, Stuart S
Hunger, Stephen P
Goossens, Steven
Castillo, Eliseo F
Ornatowski, Wojciech
Van Vlierberghe, Pieter
Matlawska-Wasowska, Ksenia
RUNX2 regulates leukemic cell metabolism and chemotaxis in high-risk T cell acute lymphoblastic leukemia.
title RUNX2 regulates leukemic cell metabolism and chemotaxis in high-risk T cell acute lymphoblastic leukemia.
title_full RUNX2 regulates leukemic cell metabolism and chemotaxis in high-risk T cell acute lymphoblastic leukemia.
title_fullStr RUNX2 regulates leukemic cell metabolism and chemotaxis in high-risk T cell acute lymphoblastic leukemia.
title_full_unstemmed RUNX2 regulates leukemic cell metabolism and chemotaxis in high-risk T cell acute lymphoblastic leukemia.
title_short RUNX2 regulates leukemic cell metabolism and chemotaxis in high-risk T cell acute lymphoblastic leukemia.
title_sort runx2 regulates leukemic cell metabolism and chemotaxis in high-risk t cell acute lymphoblastic leukemia.
topic Cell migration/adhesion
Leukemias
Molecular biology
Oncology
url http://purl.org/au-research/grants/nhmrc/1142627
http://purl.org/au-research/grants/nhmrc/1142627
http://purl.org/au-research/grants/nhmrc/1142627
http://hdl.handle.net/20.500.11937/82712