Deletion of the transcriptional regulator TFAP4 accelerates c-MYC-driven lymphomagenesis
Many lymphoid malignancies arise from deregulated c-MYC expression in cooperation with additional genetic lesions. While many of these cooperative genetic lesions have been discovered and their functions characterised, DNA sequence data of primary patient samples suggest that many more do exist. How...
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Published in | Cell death and differentiation Vol. 30; no. 6; pp. 1447 - 1456 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
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Nature Publishing Group UK
01.06.2023
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Abstract | Many lymphoid malignancies arise from deregulated c-MYC expression in cooperation with additional genetic lesions. While many of these cooperative genetic lesions have been discovered and their functions characterised, DNA sequence data of primary patient samples suggest that many more do exist. However, the nature of their contributions to c-MYC driven lymphomagenesis have not yet been investigated. We identified TFAP4 as a potent suppressor of c-MYC driven lymphoma development in a previous genome-wide CRISPR knockout screen in primary cells in vivo [
1
]. CRISPR deletion of TFAP4 in
Eµ-MYC
transgenic haematopoietic stem and progenitor cells (HSPCs) and transplantation of these manipulated HSPCs into lethally irradiated animals significantly accelerated c-MYC-driven lymphoma development. Interestingly, TFAP4 deficient
Eµ-MYC
lymphomas all arose at the pre-B cell stage of B cell development. This observation prompted us to characterise the transcriptional profile of pre-B cells from pre-leukaemic mice transplanted with
Eµ-MYC/Cas9
HSPCs that had been transduced with sgRNAs targeting TFAP4. This analysis revealed that TFAP4 deletion reduced expression of several master regulators of B cell differentiation, such as
Spi1
,
SpiB
and
Pax5
, which are direct target genes of both TFAP4 and MYC. We therefore conclude that loss of TFAP4 leads to a block in differentiation during early B cell development, thereby accelerating c-MYC-driven lymphoma development. |
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AbstractList | Many lymphoid malignancies arise from deregulated c-MYC expression in cooperation with additional genetic lesions. While many of these cooperative genetic lesions have been discovered and their functions characterised, DNA sequence data of primary patient samples suggest that many more do exist. However, the nature of their contributions to c-MYC driven lymphomagenesis have not yet been investigated. We identified TFAP4 as a potent suppressor of c-MYC driven lymphoma development in a previous genome-wide CRISPR knockout screen in primary cells in vivo [1]. CRISPR deletion of TFAP4 in Eµ-MYC transgenic haematopoietic stem and progenitor cells (HSPCs) and transplantation of these manipulated HSPCs into lethally irradiated animals significantly accelerated c-MYC-driven lymphoma development. Interestingly, TFAP4 deficient Eµ-MYC lymphomas all arose at the pre-B cell stage of B cell development. This observation prompted us to characterise the transcriptional profile of pre-B cells from pre-leukaemic mice transplanted with Eµ-MYC/Cas9 HSPCs that had been transduced with sgRNAs targeting TFAP4. This analysis revealed that TFAP4 deletion reduced expression of several master regulators of B cell differentiation, such as Spi1, SpiB and Pax5, which are direct target genes of both TFAP4 and MYC. We therefore conclude that loss of TFAP4 leads to a block in differentiation during early B cell development, thereby accelerating c-MYC-driven lymphoma development. Many lymphoid malignancies arise from deregulated c-MYC expression in cooperation with additional genetic lesions. While many of these cooperative genetic lesions have been discovered and their functions characterised, DNA sequence data of primary patient samples suggest that many more do exist. However, the nature of their contributions to c-MYC driven lymphomagenesis have not yet been investigated. We identified TFAP4 as a potent suppressor of c-MYC driven lymphoma development in a previous genome-wide CRISPR knockout screen in primary cells in vivo [ 1 ]. CRISPR deletion of TFAP4 in Eµ-MYC transgenic haematopoietic stem and progenitor cells (HSPCs) and transplantation of these manipulated HSPCs into lethally irradiated animals significantly accelerated c-MYC-driven lymphoma development. Interestingly, TFAP4 deficient Eµ-MYC lymphomas all arose at the pre-B cell stage of B cell development. This observation prompted us to characterise the transcriptional profile of pre-B cells from pre-leukaemic mice transplanted with Eµ-MYC/Cas9 HSPCs that had been transduced with sgRNAs targeting TFAP4. This analysis revealed that TFAP4 deletion reduced expression of several master regulators of B cell differentiation, such as Spi1 , SpiB and Pax5 , which are direct target genes of both TFAP4 and MYC. We therefore conclude that loss of TFAP4 leads to a block in differentiation during early B cell development, thereby accelerating c-MYC-driven lymphoma development. Many lymphoid malignancies arise from deregulated c-MYC expression in cooperation with additional genetic lesions. While many of these cooperative genetic lesions have been discovered and their functions characterised, DNA sequence data of primary patient samples suggest that many more do exist. However, the nature of their contributions to c-MYC driven lymphomagenesis have not yet been investigated. We identified TFAP4 as a potent suppressor of c-MYC driven lymphoma development in a previous genome-wide CRISPR knockout screen in primary cells in vivo [1]. CRISPR deletion of TFAP4 in Eµ-MYC transgenic haematopoietic stem and progenitor cells (HSPCs) and transplantation of these manipulated HSPCs into lethally irradiated animals significantly accelerated c-MYC-driven lymphoma development. Interestingly, TFAP4 deficient Eµ-MYC lymphomas all arose at the pre-B cell stage of B cell development. This observation prompted us to characterise the transcriptional profile of pre-B cells from pre-leukaemic mice transplanted with Eµ-MYC/Cas9 HSPCs that had been transduced with sgRNAs targeting TFAP4. This analysis revealed that TFAP4 deletion reduced expression of several master regulators of B cell differentiation, such as Spi1 , SpiB and Pax5 , which are direct target genes of both TFAP4 and MYC. We therefore conclude that loss of TFAP4 leads to a block in differentiation during early B cell development, thereby accelerating c-MYC-driven lymphoma development. |
Author | Strasser, Andreas Li Wai Suen, Connie S. N. Herold, Marco J. Tai, Lin Garnham, Alexandra L. Potts, Margaret A. Kueh, Andrew J. Pal, Martin Mizutani, Shinsuke |
Author_xml | – sequence: 1 givenname: Margaret A. orcidid: 0000-0001-9796-9683 surname: Potts fullname: Potts, Margaret A. organization: The Walter and Eliza Hall Institute of Medical Research, Blood Cells and Blood Cancer Division, Department of Medical Biology, University of Melbourne – sequence: 2 givenname: Shinsuke surname: Mizutani fullname: Mizutani, Shinsuke organization: The Walter and Eliza Hall Institute of Medical Research, Blood Cells and Blood Cancer Division, Department of Medical Biology, University of Melbourne, Division of Hematology and Oncology, Department of Medicine, Kyoto Prefectural University of Medicine – sequence: 3 givenname: Alexandra L. surname: Garnham fullname: Garnham, Alexandra L. organization: The Walter and Eliza Hall Institute of Medical Research, Blood Cells and Blood Cancer Division, Department of Medical Biology, University of Melbourne – sequence: 4 givenname: Connie S. N. orcidid: 0000-0003-0529-0804 surname: Li Wai Suen fullname: Li Wai Suen, Connie S. N. organization: The Walter and Eliza Hall Institute of Medical Research, Blood Cells and Blood Cancer Division, Department of Medical Biology, University of Melbourne – sequence: 5 givenname: Andrew J. surname: Kueh fullname: Kueh, Andrew J. organization: The Walter and Eliza Hall Institute of Medical Research, Blood Cells and Blood Cancer Division, Department of Medical Biology, University of Melbourne – sequence: 6 givenname: Lin surname: Tai fullname: Tai, Lin organization: The Walter and Eliza Hall Institute of Medical Research, Blood Cells and Blood Cancer Division – sequence: 7 givenname: Martin surname: Pal fullname: Pal, Martin organization: The Walter and Eliza Hall Institute of Medical Research, Blood Cells and Blood Cancer Division, Department of Medical Biology, University of Melbourne, School of Dentistry and Medical Sciences, Charles Sturt University – sequence: 8 givenname: Andreas orcidid: 0000-0002-5020-4891 surname: Strasser fullname: Strasser, Andreas organization: The Walter and Eliza Hall Institute of Medical Research, Blood Cells and Blood Cancer Division, Department of Medical Biology, University of Melbourne – sequence: 9 givenname: Marco J. orcidid: 0000-0001-7539-7581 surname: Herold fullname: Herold, Marco J. email: herold@wehi.edu.au organization: The Walter and Eliza Hall Institute of Medical Research, Blood Cells and Blood Cancer Division, Department of Medical Biology, University of Melbourne |
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Title | Deletion of the transcriptional regulator TFAP4 accelerates c-MYC-driven lymphomagenesis |
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