Single-cell RNA sequencing of a new transgenic t(8;21) preleukemia mouse model reveals regulatory networks promoting leukemic transformation.


Journal

Leukemia
ISSN: 1476-5551
Titre abrégé: Leukemia
Pays: England
ID NLM: 8704895

Informations de publication

Date de publication:
14 Oct 2023
Historique:
received: 24 04 2023
accepted: 05 10 2023
revised: 22 09 2023
medline: 15 10 2023
pubmed: 15 10 2023
entrez: 14 10 2023
Statut: aheadofprint

Résumé

T(8;21)(q22;q22), which generates the AML1-ETO fusion oncoprotein, is a common chromosomal abnormality in acute myeloid leukemia (AML) patients. Despite having favorable prognosis, 40% of patients will relapse, highlighting the need for innovative models and application of the newest technologies to study t(8;21) leukemogenesis. Currently, available AML1-ETO mouse models have limited utility for studying the pre-leukemic stage because AML1-ETO produces mild hematopoietic phenotypes and no leukemic transformation. Conversely, overexpression of a truncated variant, AML1-ETO9a (AE9a), promotes fully penetrant leukemia and is too potent for studying pre-leukemic changes. To overcome these limitations, we devised a germline-transmitted Rosa26 locus AE9a knock-in mouse model that moderately overexpressed AE9a and developed leukemia with long latency and low penetrance. We observed pre-leukemic alterations in AE9a mice, including skewing of progenitors towards granulocyte/monocyte lineages and replating of stem and progenitor cells. Next, we performed single-cell RNA sequencing to identify specific cell populations that contribute to these pre-leukemic phenotypes. We discovered a subset of common myeloid progenitors that have heightened granulocyte/monocyte bias in AE9a mice. We also observed dysregulation of key hematopoietic transcription factor target gene networks, blocking cellular differentiation. Finally, we identified Sox4 activation as a potential contributor to stem cell self-renewal during the pre-leukemic stage.

Identifiants

pubmed: 37838757
doi: 10.1038/s41375-023-02063-z
pii: 10.1038/s41375-023-02063-z
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI)
ID : R01CA104509
Organisme : U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI)
ID : P30CA23100
Organisme : U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI)
ID : T32CA009523
Organisme : U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI)
ID : T32CA009523

Informations de copyright

© 2023. The Author(s).

Références

Byrd JC, Mrozek K, Dodge RK, Carroll AJ, Edwards CG, Arthur DC, et al. Pretreatment cytogenetic abnormalities are predictive of induction success, cumulative incidence of relapse, and overall survival in adult patients with de novo acute myeloid leukemia: results from Cancer and Leukemia Group B (CALGB 8461). Blood. 2002;100:4325–36.
pubmed: 12393746 doi: 10.1182/blood-2002-03-0772
Dohner H, Estey E, Grimwade D, Amadori S, Appelbaum FR, Buchner T, et al. Diagnosis and management of AML in adults: 2017 ELN recommendations from an international expert panel. Blood. 2017;129:424–47.
pubmed: 27895058 pmcid: 5291965 doi: 10.1182/blood-2016-08-733196
Marcucci G, Mrozek K, Ruppert AS, Maharry K, Kolitz JE, Moore JO, et al. Prognostic factors and outcome of core binding factor acute myeloid leukemia patients with t(8;21) differ from those of patients with inv(16): a cancer and leukemia group B study. J Clin Oncol. 2005;23:5705–17.
pubmed: 16110030 doi: 10.1200/JCO.2005.15.610
Christen F, Hoyer K, Yoshida K, Hou HA, Waldhueter N, Heuser M, et al. Genomic landscape and clonal evolution of acute myeloid leukemia with t(8;21): an international study on 331 patients. Blood. 2019;133:1140–51.
pubmed: 30610028 doi: 10.1182/blood-2018-05-852822
Miyoshi H, Shimizu K, Kozu T, Maseki N, Kaneko Y, Ohki M. t(8;21) breakpoints on chromosome 21 in acute myeloid leukemia are clustered within a limited region of a single gene, AML1. Proc Natl Acad Sci USA. 1991;88:10431–4.
pubmed: 1720541 pmcid: 52942 doi: 10.1073/pnas.88.23.10431
Erickson P, Gao J, Chang KS, Look T, Whisenant E, Raimondi S, et al. Identification of breakpoints in t(8;21) acute myelogenous leukemia and isolation of a fusion transcript, AML1/ETO, with similarity to Drosophila segmentation gene, runt. Blood. 1992;80:1825–31.
pubmed: 1391946 doi: 10.1182/blood.V80.7.1825.1825
Okuda T, van Deursen J, Hiebert SW, Grosveld G, Downing JR. AML1, the target of multiple chromosomal translocations in human leukemia, is essential for normal fetal liver hematopoiesis. Cell. 1996;84:321–30.
pubmed: 8565077 doi: 10.1016/S0092-8674(00)80986-1
Growney JD, Shigematsu H, Li Z, Lee BH, Adelsperger J, Rowan R, et al. Loss of Runx1 perturbs adult hematopoiesis and is associated with a myeloproliferative phenotype. Blood. 2005;106:494–504.
pubmed: 15784726 pmcid: 1895175 doi: 10.1182/blood-2004-08-3280
Chen MJ, Yokomizo T, Zeigler B, Dzierzak E, Speck NA. Runx1 is required for the endothelial to hematopoietic cell transition but not thereafter. Nature. 2009;457:887–91.
pubmed: 19129762 pmcid: 2744041 doi: 10.1038/nature07619
Lam K, Zhang D. RUNX1 and RUNX1-ETO: roles in hematopoiesis and leukemogenesis. Front Biosci-Landmark. 2012;17:1120–39.
doi: 10.2741/3977
Gelmetti V, Zhang J, Fanelli M, Minucci S, Pelicci PG, Lazar MA. Aberrant recruitment of the nuclear receptor corepressor-histone deacetylase complex by the acute myeloid leukemia fusion partner ETO. Mol Cell Biol. 1998;18:7185–91.
pubmed: 9819405 pmcid: 109300 doi: 10.1128/MCB.18.12.7185
Lutterbach B, Westendorf JJ, Linggi B, Patten A, Moniwa M, Davie JR, et al. ETO, a target of t(8;21) in acute leukemia, interacts with the N-CoR and mSin3 corepressors. Mol Cell Biol. 1998;18:7176–84.
pubmed: 9819404 pmcid: 109299 doi: 10.1128/MCB.18.12.7176
Wang J, Hoshino T, Redner RL, Kajigaya S, Liu JM. ETO, fusion partner in t(8;21) acute myeloid leukemia, represses transcription by interaction with the human N-CoR/mSin3/HDAC1 complex. Proc Natl Acad Sci USA. 1998;95:10860–5.
pubmed: 9724795 pmcid: 27986 doi: 10.1073/pnas.95.18.10860
Okumura AJ, Peterson LF, Okumura F, Boyapati A, Zhang DE. t(8;21)(q22;q22) Fusion proteins preferentially bind to duplicated AML1/RUNX1 DNA-binding sequences to differentially regulate gene expression. Blood. 2008;112:1392–401.
pubmed: 18511808 pmcid: 2515118 doi: 10.1182/blood-2007-11-124735
Wang L, Gural A, Sun XJ, Zhao X, Perna F, Huang G, et al. The leukemogenicity of AML1-ETO is dependent on site-specific lysine acetylation. Science. 2011;333:765–9.
pubmed: 21764752 pmcid: 3251012 doi: 10.1126/science.1201662
Peterson LF, Boyapati A, Ahn EY, Biggs JR, Okumura AJ, Lo MC, et al. Acute myeloid leukemia with the 8q22;21q22 translocation: secondary mutational events and alternative t(8;21) transcripts. Blood. 2007;110:799–805.
pubmed: 17412887 pmcid: 1924771 doi: 10.1182/blood-2006-11-019265
Lindberg SR, Olsson A, Persson AM, Olsson I. The Leukemia-associated ETO homologs are differently expressed during hematopoietic differentiation. Exp Hematol. 2005;33:189–98.
pubmed: 15676213 doi: 10.1016/j.exphem.2004.10.011
Klampfer L, Zhang J, Zelenetz AO, Uchida H, Nimer SD. The AML1/ETO fusion protein activates transcription of BCL-2. Proc Natl Acad Sci USA. 1996;93:14059–64.
pubmed: 8943060 pmcid: 19494 doi: 10.1073/pnas.93.24.14059
Pabst T, Mueller BU, Harakawa N, Schoch C, Haferlach T, Behre G, et al. AML1-ETO downregulates the granulocytic differentiation factor C/EBPalpha in t(8;21) myeloid leukemia. Nat Med. 2001;7:444–51.
pubmed: 11283671 doi: 10.1038/86515
Vangala RK, Heiss-Neumann MS, Rangatia JS, Singh SM, Schoch C, Tenen DG, et al. The myeloid master regulator transcription factor PU.1 is inactivated by AML1-ETO in t(8;21) myeloid leukemia. Blood. 2003;101:270–7.
pubmed: 12393465 doi: 10.1182/blood-2002-04-1288
Ptasinska A, Assi SA, Martinez-Soria N, Imperato MR, Piper J, Cauchy P, et al. Identification of a dynamic core transcriptional network in t(8;21) AML that regulates differentiation block and self-renewal. Cell Rep. 2014;8:1974–88.
pubmed: 25242324 pmcid: 4487811 doi: 10.1016/j.celrep.2014.08.024
Hatlen MA, Wang L, Nimer SD. AML1-ETO driven acute leukemia: insights into pathogenesis and potential therapeutic approaches. Front Med. 2012;6:248–62.
pubmed: 22875638 doi: 10.1007/s11684-012-0206-6
Yan M, Kanbe E, Peterson LF, Boyapati A, Miao Y, Wang Y, et al. A previously unidentified alternatively spliced isoform of t(8;21) transcript promotes leukemogenesis. Nat Med. 2006;12:945–9.
pubmed: 16892037 doi: 10.1038/nm1443
Wolford JK, Prochazka M. Structure and expression of the human MTG8/ETO gene. Gene. 1998;212:103–9.
pubmed: 9661669 doi: 10.1016/S0378-1119(98)00141-3
LaFiura KM, Edwards H, Taub JW, Matherly LH, Fontana JA, Mohamed AN, et al. Identification and characterization of novel AML1-ETO fusion transcripts in pediatric t(8;21) acute myeloid leukemia: a report from the Children’s Oncology Group. Oncogene. 2008;27:4933–42.
pubmed: 18469864 pmcid: 3763903 doi: 10.1038/onc.2008.134
Jiao B, Wu CF, Liang Y, Chen HM, Xiong SM, Chen B, et al. AML1-ETO9a is correlated with C-KIT overexpression/mutations and indicates poor disease outcome in t(8;21) acute myeloid leukemia-M2. Leukemia. 2009;23:1598–604.
pubmed: 19458628 doi: 10.1038/leu.2009.104
Ommen HB, Ostergaard M, Yan M, Braendstrup K, Zhang DE, Hokland P. Persistent altered fusion transcript splicing identifies RUNX1-RUNX1T1+ AML patients likely to relapse. Eur J Haematol. 2010;84:128–32.
pubmed: 19891700 doi: 10.1111/j.1600-0609.2009.01371.x
Faber ZJ, Chen X, Gedman AL, Boggs K, Cheng J, Ma J, et al. The genomic landscape of core-binding factor acute myeloid leukemias. Nat Genet. 2016;48:1551–6.
pubmed: 27798625 pmcid: 5508996 doi: 10.1038/ng.3709
Agrawal M, Schwarz P, Giaimo BD, Bedzhov I, Corbacioglu A, Weber D, et al. Functional and clinical characterization of the alternatively spliced isoform AML1-ETO9a in adult patients with translocation t(8;21)(q22;q22.1) acute myeloid leukemia (AML). Leukemia. 2020;34:630–4.
pubmed: 31462736 doi: 10.1038/s41375-019-0551-4
Thiel VN, Giaimo BD, Schwarz P, Soller K, Vas V, Bartkuhn M, et al. Heterodimerization of AML1/ETO with CBFβ is required for leukemogenesis but not for myeloproliferation. Leukemia. 2017;31:2491–502.
pubmed: 28360416 pmcid: 5668496 doi: 10.1038/leu.2017.105
Link KA, Lin S, Shrestha M, Bowman M, Wunderlich M, Bloomfield CD, et al. Supraphysiologic levels of the AML1-ETO isoform AE9a are essential for transformation. Proc Natl Acad Sci USA. 2016;113:9075–80.
pubmed: 27457952 pmcid: 4987773 doi: 10.1073/pnas.1524225113
Du Y, Spence SE, Jenkins NA, Copeland NG. Cooperating cancer-gene identification through oncogenic-retrovirus-induced insertional mutagenesis. Blood. 2005;106:2498–505.
pubmed: 15961513 pmcid: 1895273 doi: 10.1182/blood-2004-12-4840
Touw IP, Erkeland SJ. Retroviral insertion mutagenesis in mice as a comparative oncogenomics tool to identify disease genes in human leukemia. Mol Ther. 2007;15:13–19.
pubmed: 17164770 doi: 10.1038/sj.mt.6300040
Piovan C, Amari F, Lovat F, Chen Q, Coppola V. Generation of mouse lines conditionally over-expressing microRNA using the Rosa26-Lox-Stop-Lox system. Methods Mol Biol. 2014;1194:203–24.
pubmed: 25064105 doi: 10.1007/978-1-4939-1215-5_11
Kita K, Shirakawa S, Kamada N. Cellular characteristics of acute myeloblastic leukemia associated with t(8;21)(q22;q22). The Japanese Cooperative Group of Leukemia/Lymphoma. Leuk Lymphoma. 1994;13:229–34.
pubmed: 8049646 doi: 10.3109/10428199409056286
Schlenk RF, Benner A, Krauter J, Büchner T, Sauerland C, Ehninger G, et al. Individual patient data-based meta-analysis of patients aged 16–60 years with core binding factor acute myeloid leukemia: a survey of the German Acute Myeloid Leukemia Intergroup. J Clin Oncol. 2004;22:3741–50.
pubmed: 15289486 doi: 10.1200/JCO.2004.03.012
Cabezas-Wallscheid N, Klimmeck D, Hansson J, Lipka DB, Reyes A, Wang Q, et al. Identification of regulatory networks in HSCs and their immediate progeny via integrated proteome, transcriptome, and DNA methylome analysis. Cell Stem Cell. 2014;15:507–22.
pubmed: 25158935 doi: 10.1016/j.stem.2014.07.005
Pietras EM, Reynaud D, Kang YA, Carlin D, Calero-Nieto FJ, Leavitt AD, et al. Functionally distinct subsets of lineage-biased multipotent progenitors control blood production in normal and regenerative conditions. Cell Stem Cell. 2015;17:35–46.
pubmed: 26095048 pmcid: 4542150 doi: 10.1016/j.stem.2015.05.003
Hafemeister C, Halbritter F. Single-cell RNA-seq differential expression tests within a sample should use pseudo-bulk data of pseudo-replicates. biorXiv 2023-04-12. 2023.
Piñero J, Ramírez-Anguita JM, Saüch-Pitarch J, Ronzano F, Centeno E, Sanz F, et al. The DisGeNET knowledge platform for disease genomics: 2019 update. Nucleic Acids Res. 2020;48:D845–55.
pubmed: 31680165
Zhou Y, Zhou B, Pache L, Chang M, Khodabakhshi AH, Tanaseichuk O, et al. Metascape provides a biologist-oriented resource for the analysis of systems-level datasets. Nat Commun. 2019;10:1523.
doi: 10.1038/s41467-019-09234-6
DePasquale EAK, Schnell D, Dexheimer P, Ferchen K, Hay S, Chetal K, et al. cellHarmony: cell-level matching and holistic comparison of single-cell transcriptomes. Nucleic Acids Res. 2019;47:e138.
pubmed: 31529053 pmcid: 6868361 doi: 10.1093/nar/gkz789
Chen H, Albergante L, Hsu JY, Lareau CA, Lo Bosco G, Guan J, et al. Single-cell trajectories reconstruction, exploration, and mapping of omics data with STREAM. Nat Commun. 2019;10:1903.
pubmed: 31015418 pmcid: 6478907 doi: 10.1038/s41467-019-09670-4
Laurenti E, Doulatov S, Zandi S, Plumb I, Chen J, April C, et al. The transcriptional architecture of early human hematopoiesis identifies multilevel control of lymphoid commitment. Nat Immunol. 2013;14:756–63.
pubmed: 23708252 pmcid: 4961471 doi: 10.1038/ni.2615
Aibar S, González-Blas CB, Moerman T, Huynh-Thu VA, Imrichova H, Hulselmans G, et al. SCENIC: Single-cell regulatory network inference and clustering. Nat Methods. 2017;14:1083–6.
pubmed: 28991892 pmcid: 5937676 doi: 10.1038/nmeth.4463
Stengel KR, Ellis JD, Spielman CL, Bomber ML, Hiebert SW. Definition of a small core transcriptional circuit regulated by AML1-ETO. Mol Cell. 2021;81:530–45.
pubmed: 33382982 doi: 10.1016/j.molcel.2020.12.005
Deneault E, Cellot S, Faubert A, Laverdure JP, Fréchette M, Chagraoui J, et al. A functional screen to identify novel effectors of hematopoietic stem cell activity. Cell. 2009;137:369–79.
pubmed: 19379700 pmcid: 5770201 doi: 10.1016/j.cell.2009.03.026
Lu JW, Hsieh MS, Hou HA, Chen CY, Tien HF, Lin LI. Overexpression of SOX4 correlates with poor prognosis of acute myeloid leukemia and is leukemogenic in zebrafish. Blood Cancer J. 2017;7:e593.
pubmed: 28841206 pmcid: 5596385 doi: 10.1038/bcj.2017.74
Sandoval S, Kraus C, Cho EC, Cho M, Bies J, Manara E, et al. Sox4 cooperates with CREB in myeloid transformation. Blood. 2012;120:155–65.
pubmed: 22627767 pmcid: 3390953 doi: 10.1182/blood-2011-05-357418
Ramezani-Rad P, Geng H, Hurtz C, Chan LN, Chen Z, Jumaa H, et al. SOX4 enables oncogenic survival signals in acute lymphoblastic leukemia. Blood. 2013;121:148–55.
pubmed: 23152540 pmcid: 3538327 doi: 10.1182/blood-2012-05-428938
Berger R, Bernheim A, Daniel MT, Valensi F, Sigaux F, Flandrin G. Cytologic characterization and significance of normal karyotypes in t(8;21) acute myeloblastic leukemia. Blood. 1982;59:171–8.
pubmed: 6947830 doi: 10.1182/blood.V59.1.171.171
Swirsky DM, Li YS, Matthews JG, Flemans RJ, Rees JK, Hayhoe FG. 8;21 translocation in acute granulocytic leukemia: cytological, cytochemical and clinical features. Br J Haematol. 1984;56:199–213.
pubmed: 6197988 doi: 10.1111/j.1365-2141.1984.tb03948.x
Yeh JR, Munson KM, Chao YL, Peterson QP, Macrae CA, Peterson RT. AML1-ETO reprograms hematopoietic cell fate by downregulating scl expression. Development. 2008;135:401–10.
pubmed: 18156164 doi: 10.1242/dev.008904
Schwieger M, Lohler J, Friel J, Scheller M, Horak I, Stocking C. AML1-ETO inhibits maturation of multiple lymphohematopoietic lineages and induces myeloblast transformation in synergy with ICSBP deficiency. J Exp Med. 2002;196:1227–40.
pubmed: 12417632 pmcid: 2194108 doi: 10.1084/jem.20020824
Fenske TS, Pengue G, Mathews V, Hanson PT, Hamm SE, Riaz N, et al. Stem cell expression of the AML1/ETO fusion protein induces a myeloproliferative disorder in mice. Proc Natl Acad Sci USA. 2004;101:15184–9.
pubmed: 15477599 pmcid: 524043 doi: 10.1073/pnas.0400751101
Choi Y, Elagib KE, Delehanty LL, Goldfarb AN. Erythroid inhibition by the leukemic fusion AML1-ETO is associated with impaired acetylation of the major erythroid transcription factor GATA-1. Cancer Res. 2006;66:2990–6.
pubmed: 16540647 doi: 10.1158/0008-5472.CAN-05-2944
Nimer SD, Moore MA. Effects of the leukemia-associated AML1-ETO protein on hematopoietic stem and progenitor cells. Oncogene. 2004;23:4249–54.
pubmed: 15156180 doi: 10.1038/sj.onc.1207673
Zhang H, Alberich-Jorda M, Amabile G, Yang H, Staber PB, Di Ruscio A, et al. Sox4 is a key oncogenic target in C/EBPα mutant acute myeloid leukemia. Cancer Cell. 2013;24:575–88.
pubmed: 24183681 pmcid: 4038627 doi: 10.1016/j.ccr.2013.09.018
Nafria M, Keane P, Ng ES, Stanley EG, Elefanty AG, Bonifer C. Expression of RUNX1-ETO rapidly alters the chromatin landscape and growth of early human myeloid precursor cells. Cell Rep. 2020;31:107691.
pubmed: 32460028 pmcid: 7262600 doi: 10.1016/j.celrep.2020.107691
Tonks A, Pearn L, Musson M, Gilkes A, Mills KI, Burnett AK, et al. Transcriptional dysregulation mediated by RUNX1-RUNX1T1 in normal human progenitor cells and in acute myeloid leukemia. Leukemia. 2007;21:2495–505.
pubmed: 17898786 doi: 10.1038/sj.leu.2404961
Bagger FO, Kinalis S, Rapin N. BloodSpot: a database of healthy and malignant hematopoiesis updated with purified and single-cell mRNA sequencing profiles. Nucleic Acids Res. 2019;47:D881–5.
pubmed: 30395307 doi: 10.1093/nar/gky1076

Auteurs

Ming Yan (M)

Moores Cancer Center, University of California San Diego, La Jolla, CA, USA.
Department of Pathology, University of California San Diego, La Jolla, CA, USA.

Mengdan Liu (M)

Moores Cancer Center, University of California San Diego, La Jolla, CA, USA.
Department of Pathology, University of California San Diego, La Jolla, CA, USA.
School of Biological Sciences, University of California San Diego, La Jolla, CA, USA.

Amanda G Davis (AG)

Moores Cancer Center, University of California San Diego, La Jolla, CA, USA.
Department of Pathology, University of California San Diego, La Jolla, CA, USA.

Samuel A Stoner (SA)

Moores Cancer Center, University of California San Diego, La Jolla, CA, USA.

Dong-Er Zhang (DE)

Moores Cancer Center, University of California San Diego, La Jolla, CA, USA. dez@ucsd.edu.
Department of Pathology, University of California San Diego, La Jolla, CA, USA. dez@ucsd.edu.
School of Biological Sciences, University of California San Diego, La Jolla, CA, USA. dez@ucsd.edu.

Classifications MeSH