Graphdiyne oxide nanosheets display selective anti-leukemia efficacy against DNMT3A-mutant AML cells

DNA methyltransferase 3 A ( DNMT3A ) is the most frequently mutated gene in acute myeloid leukemia (AML). Although chemotherapy agents have improved outcomes for DNMT3A -mutant AML patients, there is still no targeted therapy highlighting the need for further study of how DNMT3A mutations affect AML...

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Published inNature communications Vol. 13; no. 1; pp. 5657 - 16
Main Authors Wang, Qiwei, Liu, Ying, Wang, Hui, Jiang, Penglei, Qian, Wenchang, You, Min, Han, Yingli, Zeng, Xin, Li, Jinxin, Lu, Huan, Jiang, Lingli, Zhu, Meng, Li, Shilin, Huang, Kang, Tang, Mingmin, Wang, Xinlian, Yan, Liang, Xiong, Zecheng, Shi, Xinghua, Bai, Ge, Liu, Huibiao, Li, Yuliang, Zhao, Yuliang, Chen, Chunying, Qian, Pengxu
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 26.09.2022
Nature Publishing Group
Nature Portfolio
Subjects
13/31
14/19
14/28
14/5
38/91
631/154/155
631/67/1059/602
692/4028/67/1059/153
692/4028/67/1990/283/1897
82/58
Actin
Acute myeloid leukemia
Age
Apoptosis
Blood cancer
Cell adhesion
Chemotherapy
Cytoskeleton
Deoxyribonucleic acid
DNA
DNA methyltransferase
Drug development
Humanities and Social Sciences
Leukemia
Mannose
multidisciplinary
Mutants
Mutation
Nanomaterials
Nanosheets
Nanotechnology
Phenotypes
Science
Science (multidisciplinary)
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Abstract DNA methyltransferase 3 A ( DNMT3A ) is the most frequently mutated gene in acute myeloid leukemia (AML). Although chemotherapy agents have improved outcomes for DNMT3A -mutant AML patients, there is still no targeted therapy highlighting the need for further study of how DNMT3A mutations affect AML phenotype. Here, we demonstrate that cell adhesion-related genes are predominantly enriched in DNMT3A -mutant AML cells and identify that graphdiyne oxide (GDYO) display an anti-leukemia effect specifically against these mutated cells. Mechanistically, GDYO directly interacts with integrin β2 (ITGB2) and c-type mannose receptor (MRC2), which facilitate the attachment and cellular uptake of GDYO. Furthermore, GDYO binds to actin and prevents actin polymerization, thus disrupting the actin cytoskeleton and eventually leading to cell apoptosis. Finally, we validate the in vivo safety and therapeutic potential of GDYO against DNMT3A -mutant AML cells. Collectively, these findings demonstrate that GDYO is an efficient and specific drug candidate against DNMT3A -mutant AML. DNA methyltransferase 3A, a mutated gene associated with hematologic malignancies in age-related clonal haematopoiesis lacks targeted therapies. Here, the authors screen carbon nanomaterials and find graphdiyne oxide binds to mutant cells and disrupts cellular processes with a therapeutic effect in vitro and in vivo.
AbstractList DNA methyltransferase 3 A ( DNMT3A ) is the most frequently mutated gene in acute myeloid leukemia (AML). Although chemotherapy agents have improved outcomes for DNMT3A -mutant AML patients, there is still no targeted therapy highlighting the need for further study of how DNMT3A mutations affect AML phenotype. Here, we demonstrate that cell adhesion-related genes are predominantly enriched in DNMT3A -mutant AML cells and identify that graphdiyne oxide (GDYO) display an anti-leukemia effect specifically against these mutated cells. Mechanistically, GDYO directly interacts with integrin β2 (ITGB2) and c-type mannose receptor (MRC2), which facilitate the attachment and cellular uptake of GDYO. Furthermore, GDYO binds to actin and prevents actin polymerization, thus disrupting the actin cytoskeleton and eventually leading to cell apoptosis. Finally, we validate the in vivo safety and therapeutic potential of GDYO against DNMT3A -mutant AML cells. Collectively, these findings demonstrate that GDYO is an efficient and specific drug candidate against DNMT3A -mutant AML.
DNA methyltransferase 3 A (DNMT3A) is the most frequently mutated gene in acute myeloid leukemia (AML). Although chemotherapy agents have improved outcomes for DNMT3A-mutant AML patients, there is still no targeted therapy highlighting the need for further study of how DNMT3A mutations affect AML phenotype. Here, we demonstrate that cell adhesion-related genes are predominantly enriched in DNMT3A-mutant AML cells and identify that graphdiyne oxide (GDYO) display an anti-leukemia effect specifically against these mutated cells. Mechanistically, GDYO directly interacts with integrin β2 (ITGB2) and c-type mannose receptor (MRC2), which facilitate the attachment and cellular uptake of GDYO. Furthermore, GDYO binds to actin and prevents actin polymerization, thus disrupting the actin cytoskeleton and eventually leading to cell apoptosis. Finally, we validate the in vivo safety and therapeutic potential of GDYO against DNMT3A-mutant AML cells. Collectively, these findings demonstrate that GDYO is an efficient and specific drug candidate against DNMT3A-mutant AML.DNA methyltransferase 3A, a mutated gene associated with hematologic malignancies in age-related clonal haematopoiesis lacks targeted therapies. Here, the authors screen carbon nanomaterials and find graphdiyne oxide binds to mutant cells and disrupts cellular processes with a therapeutic effect in vitro and in vivo.
DNA methyltransferase 3 A (DNMT3A) is the most frequently mutated gene in acute myeloid leukemia (AML). Although chemotherapy agents have improved outcomes for DNMT3A-mutant AML patients, there is still no targeted therapy highlighting the need for further study of how DNMT3A mutations affect AML phenotype. Here, we demonstrate that cell adhesion-related genes are predominantly enriched in DNMT3A-mutant AML cells and identify that graphdiyne oxide (GDYO) display an anti-leukemia effect specifically against these mutated cells. Mechanistically, GDYO directly interacts with integrin β2 (ITGB2) and c-type mannose receptor (MRC2), which facilitate the attachment and cellular uptake of GDYO. Furthermore, GDYO binds to actin and prevents actin polymerization, thus disrupting the actin cytoskeleton and eventually leading to cell apoptosis. Finally, we validate the in vivo safety and therapeutic potential of GDYO against DNMT3A-mutant AML cells. Collectively, these findings demonstrate that GDYO is an efficient and specific drug candidate against DNMT3A-mutant AML.DNA methyltransferase 3 A (DNMT3A) is the most frequently mutated gene in acute myeloid leukemia (AML). Although chemotherapy agents have improved outcomes for DNMT3A-mutant AML patients, there is still no targeted therapy highlighting the need for further study of how DNMT3A mutations affect AML phenotype. Here, we demonstrate that cell adhesion-related genes are predominantly enriched in DNMT3A-mutant AML cells and identify that graphdiyne oxide (GDYO) display an anti-leukemia effect specifically against these mutated cells. Mechanistically, GDYO directly interacts with integrin β2 (ITGB2) and c-type mannose receptor (MRC2), which facilitate the attachment and cellular uptake of GDYO. Furthermore, GDYO binds to actin and prevents actin polymerization, thus disrupting the actin cytoskeleton and eventually leading to cell apoptosis. Finally, we validate the in vivo safety and therapeutic potential of GDYO against DNMT3A-mutant AML cells. Collectively, these findings demonstrate that GDYO is an efficient and specific drug candidate against DNMT3A-mutant AML.
DNA methyltransferase 3 A ( DNMT3A ) is the most frequently mutated gene in acute myeloid leukemia (AML). Although chemotherapy agents have improved outcomes for DNMT3A -mutant AML patients, there is still no targeted therapy highlighting the need for further study of how DNMT3A mutations affect AML phenotype. Here, we demonstrate that cell adhesion-related genes are predominantly enriched in DNMT3A -mutant AML cells and identify that graphdiyne oxide (GDYO) display an anti-leukemia effect specifically against these mutated cells. Mechanistically, GDYO directly interacts with integrin β2 (ITGB2) and c-type mannose receptor (MRC2), which facilitate the attachment and cellular uptake of GDYO. Furthermore, GDYO binds to actin and prevents actin polymerization, thus disrupting the actin cytoskeleton and eventually leading to cell apoptosis. Finally, we validate the in vivo safety and therapeutic potential of GDYO against DNMT3A -mutant AML cells. Collectively, these findings demonstrate that GDYO is an efficient and specific drug candidate against DNMT3A -mutant AML. DNA methyltransferase 3A, a mutated gene associated with hematologic malignancies in age-related clonal haematopoiesis lacks targeted therapies. Here, the authors screen carbon nanomaterials and find graphdiyne oxide binds to mutant cells and disrupts cellular processes with a therapeutic effect in vitro and in vivo.
DNA methyltransferase 3A, a mutated gene associated with hematologic malignancies in age-related clonal haematopoiesis lacks targeted therapies. Here, the authors screen carbon nanomaterials and find graphdiyne oxide binds to mutant cells and disrupts cellular processes with a therapeutic effect in vitro and in vivo.
ArticleNumber 5657
Author Jiang, Lingli
Li, Jinxin
Liu, Huibiao
Xiong, Zecheng
Wang, Qiwei
Qian, Wenchang
Li, Yuliang
Wang, Xinlian
Zeng, Xin
Qian, Pengxu
Huang, Kang
You, Min
Bai, Ge
Wang, Hui
Yan, Liang
Li, Shilin
Zhao, Yuliang
Han, Yingli
Tang, Mingmin
Liu, Ying
Zhu, Meng
Lu, Huan
Chen, Chunying
Shi, Xinghua
Jiang, Penglei
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SSID ssj0000391844
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Snippet DNA methyltransferase 3 A ( DNMT3A ) is the most frequently mutated gene in acute myeloid leukemia (AML). Although chemotherapy agents have improved outcomes...
DNA methyltransferase 3 A (DNMT3A) is the most frequently mutated gene in acute myeloid leukemia (AML). Although chemotherapy agents have improved outcomes for...
DNA methyltransferase 3A, a mutated gene associated with hematologic malignancies in age-related clonal haematopoiesis lacks targeted therapies. Here, the...
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DNA methyltransferase
Drug development
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Title Graphdiyne oxide nanosheets display selective anti-leukemia efficacy against DNMT3A-mutant AML cells
URI https://link.springer.com/article/10.1038/s41467-022-33410-w
https://www.proquest.com/docview/2718022008
https://www.proquest.com/docview/2718633618
https://pubmed.ncbi.nlm.nih.gov/PMC9512932
https://doaj.org/article/ad94c52bd66b4f4090ae67d2fab038fa
Volume 13
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