UBE2J2/UBE2K-MARCH5泛素化机制调控急性髓系白血病中对维奈克拉的凋亡反应。 - Suppr

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The UBE2J2/UBE2K-MARCH5 ubiquitination machinery regulates apoptosis in response to venetoclax in acute myeloid leukemia.

作者信息

Lin Shan, Schneider Constanze, Su Angela H, Alexe Gabriela, Root David E, Stegmaier Kimberly

机构信息

Department of Pediatric Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.

Broad Institute of MIT and Harvard, Cambridge, MA, USA.

出版信息

Leukemia. 2024 Mar;38(3):652-656. doi: 10.1038/s41375-024-02178-x. Epub 2024 Feb 16.

DOI:10.1038/s41375-024-02178-x

PMID:38366087

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10912020/

Abstract

摘要

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e44a/10912020/96095e02d192/41375_2024_2178_Fig1_HTML.jpg

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The UBE2J2/UBE2K-MARCH5 ubiquitination machinery regulates apoptosis in response to venetoclax in acute myeloid leukemia.

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CD34 acute myeloid leukemia cells with low levels of reactive oxygen species show increased expression of stemness genes and can be targeted by the BCL2 inhibitor venetoclax.

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Venetoclax efficacy on acute myeloid leukemia is enhanced by the combination with butyrate.

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引用本文的文献

Role of MARCH E3 ubiquitin ligases in cancer development.

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本文引用的文献

Targeting a mitochondrial E3 ubiquitin ligase complex to overcome AML cell-intrinsic Venetoclax resistance.

Leukemia. 2023 May;37(5):1028-1038. doi: 10.1038/s41375-023-01879-z. Epub 2023 Mar 27.

An CRISPR Screening Platform for Prioritizing Therapeutic Targets in AML.

Cancer Discov. 2022 Feb;12(2):432-449. doi: 10.1158/2159-8290.CD-20-1851. Epub 2021 Sep 16.

Integrated analysis of patient samples identifies biomarkers for venetoclax efficacy and combination strategies in acute myeloid leukemia.

Nat Cancer. 2020 Aug;1(8):826-839. doi: 10.1038/s43018-020-0103-x. Epub 2020 Aug 18.

Rapid and direct control of target protein levels with VHL-recruiting dTAG molecules.

Nat Commun. 2020 Sep 18;11(1):4687. doi: 10.1038/s41467-020-18377-w.

MARCH5 requires MTCH2 to coordinate proteasomal turnover of the MCL1:NOXA complex.

Cell Death Differ. 2020 Aug;27(8):2484-2499. doi: 10.1038/s41418-020-0517-0. Epub 2020 Feb 24.

5-Azacitidine Induces NOXA to Prime AML Cells for Venetoclax-Mediated Apoptosis.

Clin Cancer Res. 2020 Jul 1;26(13):3371-3383. doi: 10.1158/1078-0432.CCR-19-1900. Epub 2020 Feb 13.

MARCH5-dependent degradation of MCL1/NOXA complexes defines susceptibility to antimitotic drug treatment.

Cell Death Differ. 2020 Aug;27(8):2297-2312. doi: 10.1038/s41418-020-0503-6. Epub 2020 Feb 3.

Monocytic Subclones Confer Resistance to Venetoclax-Based Therapy in Patients with Acute Myeloid Leukemia.

Cancer Discov. 2020 Apr;10(4):536-551. doi: 10.1158/2159-8290.CD-19-0710. Epub 2020 Jan 23.

Targeting Mitochondrial Structure Sensitizes Acute Myeloid Leukemia to Venetoclax Treatment.

Cancer Discov. 2019 Jul;9(7):890-909. doi: 10.1158/2159-8290.CD-19-0117. Epub 2019 May 2.

The BCL-2 arbiters of apoptosis and their growing role as cancer targets.

Cell Death Differ. 2018 Jan;25(1):27-36. doi: 10.1038/cdd.2017.161. Epub 2017 Nov 3.

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The UBE2J2/UBE2K-MARCH5 ubiquitination machinery regulates apoptosis in response to venetoclax in acute myeloid leukemia.

作者信息

Lin Shan, Schneider Constanze, Su Angela H, Alexe Gabriela, Root David E, Stegmaier Kimberly

机构信息

Department of Pediatric Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.

Broad Institute of MIT and Harvard, Cambridge, MA, USA.

出版信息

Leukemia. 2024 Mar;38(3):652-656. doi: 10.1038/s41375-024-02178-x. Epub 2024 Feb 16.

DOI:10.1038/s41375-024-02178-x

PMID:38366087

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10912020/

Abstract

摘要

相似文献

The UBE2J2/UBE2K-MARCH5 ubiquitination machinery regulates apoptosis in response to venetoclax in acute myeloid leukemia.

Leukemia. 2024 Mar;38(3):652-656. doi: 10.1038/s41375-024-02178-x. Epub 2024 Feb 16.

Targeting a mitochondrial E3 ubiquitin ligase complex to overcome AML cell-intrinsic Venetoclax resistance.

Leukemia. 2023 May;37(5):1028-1038. doi: 10.1038/s41375-023-01879-z. Epub 2023 Mar 27.

Venetoclax Synergistically Enhances the Anti-leukemic Activity of Vosaroxin Against Acute Myeloid Leukemia Cells Ex Vivo.

Target Oncol. 2019 Jun;14(3):351-364. doi: 10.1007/s11523-019-00638-4.

Enhancing venetoclax activity in acute myeloid leukemia by co-targeting MCL1.

Leukemia. 2018 Feb;32(2):303-312. doi: 10.1038/leu.2017.243. Epub 2017 Jul 28.

The Bcl-2 inhibitor venetoclax inhibits Nrf2 antioxidant pathway activation induced by hypomethylating agents in AML.

J Cell Physiol. 2019 Aug;234(8):14040-14049. doi: 10.1002/jcp.28091. Epub 2019 Jan 8.

Venetoclax resistance in acute myeloid leukaemia-Clinical and biological insights.

Br J Haematol. 2024 Apr;204(4):1146-1158. doi: 10.1111/bjh.19314. Epub 2024 Jan 31.

Prospects for Venetoclax in Myelodysplastic Syndromes.

Hematol Oncol Clin North Am. 2020 Apr;34(2):441-448. doi: 10.1016/j.hoc.2019.10.005. Epub 2019 Dec 11.

CD34 acute myeloid leukemia cells with low levels of reactive oxygen species show increased expression of stemness genes and can be targeted by the BCL2 inhibitor venetoclax.

Haematologica. 2020 Aug;105(8):e399-e403. doi: 10.3324/haematol.2019.229997. Epub 2019 Nov 14.

Venetoclax efficacy on acute myeloid leukemia is enhanced by the combination with butyrate.

Sci Rep. 2024 Feb 29;14(1):4975. doi: 10.1038/s41598-024-55286-0.

Acute myeloid leukemia-driven IL-3-dependent upregulation of BCL2 in non-malignant hematopoietic stem and progenitor cells increases venetoclax-induced cytopenias.

Haematologica. 2024 May 1;109(5):1576-1581. doi: 10.3324/haematol.2023.283944.

引用本文的文献

Role of MARCH E3 ubiquitin ligases in cancer development.

Cancer Metastasis Rev. 2024 Dec;43(4):1257-1277. doi: 10.1007/s10555-024-10201-x. Epub 2024 Jul 22.

本文引用的文献

Targeting a mitochondrial E3 ubiquitin ligase complex to overcome AML cell-intrinsic Venetoclax resistance.

Leukemia. 2023 May;37(5):1028-1038. doi: 10.1038/s41375-023-01879-z. Epub 2023 Mar 27.

An CRISPR Screening Platform for Prioritizing Therapeutic Targets in AML.

Cancer Discov. 2022 Feb;12(2):432-449. doi: 10.1158/2159-8290.CD-20-1851. Epub 2021 Sep 16.

Integrated analysis of patient samples identifies biomarkers for venetoclax efficacy and combination strategies in acute myeloid leukemia.

Nat Cancer. 2020 Aug;1(8):826-839. doi: 10.1038/s43018-020-0103-x. Epub 2020 Aug 18.

Rapid and direct control of target protein levels with VHL-recruiting dTAG molecules.

Nat Commun. 2020 Sep 18;11(1):4687. doi: 10.1038/s41467-020-18377-w.

MARCH5 requires MTCH2 to coordinate proteasomal turnover of the MCL1:NOXA complex.

Cell Death Differ. 2020 Aug;27(8):2484-2499. doi: 10.1038/s41418-020-0517-0. Epub 2020 Feb 24.

5-Azacitidine Induces NOXA to Prime AML Cells for Venetoclax-Mediated Apoptosis.

Clin Cancer Res. 2020 Jul 1;26(13):3371-3383. doi: 10.1158/1078-0432.CCR-19-1900. Epub 2020 Feb 13.

MARCH5-dependent degradation of MCL1/NOXA complexes defines susceptibility to antimitotic drug treatment.

Cell Death Differ. 2020 Aug;27(8):2297-2312. doi: 10.1038/s41418-020-0503-6. Epub 2020 Feb 3.

Monocytic Subclones Confer Resistance to Venetoclax-Based Therapy in Patients with Acute Myeloid Leukemia.

Cancer Discov. 2020 Apr;10(4):536-551. doi: 10.1158/2159-8290.CD-19-0710. Epub 2020 Jan 23.

Targeting Mitochondrial Structure Sensitizes Acute Myeloid Leukemia to Venetoclax Treatment.

Cancer Discov. 2019 Jul;9(7):890-909. doi: 10.1158/2159-8290.CD-19-0117. Epub 2019 May 2.

The BCL-2 arbiters of apoptosis and their growing role as cancer targets.

Cell Death Differ. 2018 Jan;25(1):27-36. doi: 10.1038/cdd.2017.161. Epub 2017 Nov 3.