载脂蛋白B mRNA编辑酶催化多肽样蛋白3（APOBEC3）上调导致吉西他滨耐药。 - Suppr

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超能文献

APOBEC3 upregulation drives gemcitabine resistance.

作者信息

Maciejowski John, Mohamed Taha

机构信息

Memorial Sloan Kettering Cancer Center, New York, NY, USA.

出版信息

Nat Cancer. 2024 Jun;5(6):818-820. doi: 10.1038/s43018-024-00755-8.

DOI:10.1038/s43018-024-00755-8

PMID:38778178

Abstract

摘要

相似文献

APOBEC3 upregulation drives gemcitabine resistance.

Nat Cancer. 2024 Jun;5(6):818-820. doi: 10.1038/s43018-024-00755-8.

Is the resistance of gemcitabine for pancreatic cancer settled only by overexpression of deoxycytidine kinase?

Oncol Rep. 2010 Feb;23(2):471-5.

MiR-608 regulating the expression of ribonucleotide reductase M1 and cytidine deaminase is repressed through induced gemcitabine chemoresistance in pancreatic cancer cells.

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Cytidine deaminases APOBEC3C and APOBEC3D promote DNA replication stress resistance in pancreatic cancer cells.

Nat Cancer. 2024 Jun;5(6):895-915. doi: 10.1038/s43018-024-00742-z. Epub 2024 Mar 6.

Forced expression of cytidine deaminase confers resistance to cytosine arabinoside and gemcitabine.

Exp Hematol. 1996 Sep;24(11):1340-6.

Interdependence of gemcitabine treatment, transporter expression, and resistance in human pancreatic carcinoma cells.

Neoplasia. 2010 Sep;12(9):740-7. doi: 10.1593/neo.10576.

[Expression of Gemcitabine-resistance-related gene and polymorphism of ribonucleotide reductase M1 gene promoter in Gemcitabine-resistant A549/Gem and NCI-H460/Gem cell lines].

Zhonghua Zhong Liu Za Zhi. 2010 Jan;32(1):17-21.

Macrophages mediate gemcitabine resistance of pancreatic adenocarcinoma by upregulating cytidine deaminase.

Oncogene. 2014 Jul 17;33(29):3812-9. doi: 10.1038/onc.2013.357. Epub 2013 Sep 2.

Role of deoxycytidine kinase (dCK), thymidine kinase 2 (TK2), and deoxycytidine deaminase (dCDA) in the antitumor activity of gemcitabine (dFdC).

Adv Exp Med Biol. 1998;431:657-60. doi: 10.1007/978-1-4615-5381-6_127.

引用本文的文献

Comparative Molecular Docking of Apigenin and Luteolin versus Conventional Ligands for TP-53, pRb, APOBEC3H, and HPV-16 E6: Potential Clinical Applications in Preventing Gynecological Malignancies.

Curr Issues Mol Biol. 2024 Oct 3;46(10):11136-11155. doi: 10.3390/cimb46100661.

本文引用的文献

The cytidine deaminase APOBEC3C has unique sequence and genome feature preferences.

Genetics. 2024 Aug 7;227(4). doi: 10.1093/genetics/iyae092.

Cytidine deaminases APOBEC3C and APOBEC3D promote DNA replication stress resistance in pancreatic cancer cells.

Nat Cancer. 2024 Jun;5(6):895-915. doi: 10.1038/s43018-024-00742-z. Epub 2024 Mar 6.

APOBEC3A induces DNA gaps through PRIMPOL and confers gap-associated therapeutic vulnerability.

Sci Adv. 2024 Jan 19;10(3):eadk2771. doi: 10.1126/sciadv.adk2771.

The role of APOBEC3B in lung tumor evolution and targeted cancer therapy resistance.

Nat Genet. 2024 Jan;56(1):60-73. doi: 10.1038/s41588-023-01592-8. Epub 2023 Dec 4.

Human APOBEC3B promotes tumor development in vivo including signature mutations and metastases.

Cell Rep Med. 2023 Oct 17;4(10):101211. doi: 10.1016/j.xcrm.2023.101211. Epub 2023 Oct 4.

Therapy-induced APOBEC3A drives evolution of persistent cancer cells.

Nature. 2023 Aug;620(7973):393-401. doi: 10.1038/s41586-023-06303-1. Epub 2023 Jul 5.

Addressing the benefits of inhibiting APOBEC3-dependent mutagenesis in cancer.

Nat Genet. 2022 Nov;54(11):1599-1608. doi: 10.1038/s41588-022-01196-8. Epub 2022 Oct 24.

Mechanisms of APOBEC3 mutagenesis in human cancer cells.

Nature. 2022 Jul;607(7920):799-807. doi: 10.1038/s41586-022-04972-y. Epub 2022 Jul 20.

APOBEC3A drives deaminase domain-independent chromosomal instability to promote pancreatic cancer metastasis.

Nat Cancer. 2021 Dec;2(12):1338-1356. doi: 10.1038/s43018-021-00268-8. Epub 2021 Nov 18.

HMCES Maintains Replication Fork Progression and Prevents Double-Strand Breaks in Response to APOBEC Deamination and Abasic Site Formation.

Cell Rep. 2020 Jun 2;31(9):107705. doi: 10.1016/j.celrep.2020.107705.

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APOBEC3 upregulation drives gemcitabine resistance.

作者信息

Maciejowski John, Mohamed Taha

机构信息

Memorial Sloan Kettering Cancer Center, New York, NY, USA.

出版信息

Nat Cancer. 2024 Jun;5(6):818-820. doi: 10.1038/s43018-024-00755-8.

DOI:10.1038/s43018-024-00755-8

PMID:38778178

Abstract

摘要

相似文献

APOBEC3 upregulation drives gemcitabine resistance.

Nat Cancer. 2024 Jun;5(6):818-820. doi: 10.1038/s43018-024-00755-8.

Is the resistance of gemcitabine for pancreatic cancer settled only by overexpression of deoxycytidine kinase?

Oncol Rep. 2010 Feb;23(2):471-5.

MiR-608 regulating the expression of ribonucleotide reductase M1 and cytidine deaminase is repressed through induced gemcitabine chemoresistance in pancreatic cancer cells.

Cancer Chemother Pharmacol. 2017 Oct;80(4):765-775. doi: 10.1007/s00280-017-3418-2. Epub 2017 Sep 8.

Deciphering the role of Enterococcus faecium cytidine deaminase in gemcitabine resistance of gallbladder cancer.

J Biol Chem. 2024 Apr;300(4):107171. doi: 10.1016/j.jbc.2024.107171. Epub 2024 Mar 15.

Cytidine deaminases APOBEC3C and APOBEC3D promote DNA replication stress resistance in pancreatic cancer cells.

Nat Cancer. 2024 Jun;5(6):895-915. doi: 10.1038/s43018-024-00742-z. Epub 2024 Mar 6.

Forced expression of cytidine deaminase confers resistance to cytosine arabinoside and gemcitabine.

Exp Hematol. 1996 Sep;24(11):1340-6.

Interdependence of gemcitabine treatment, transporter expression, and resistance in human pancreatic carcinoma cells.

Neoplasia. 2010 Sep;12(9):740-7. doi: 10.1593/neo.10576.

[Expression of Gemcitabine-resistance-related gene and polymorphism of ribonucleotide reductase M1 gene promoter in Gemcitabine-resistant A549/Gem and NCI-H460/Gem cell lines].

Zhonghua Zhong Liu Za Zhi. 2010 Jan;32(1):17-21.

Macrophages mediate gemcitabine resistance of pancreatic adenocarcinoma by upregulating cytidine deaminase.

Oncogene. 2014 Jul 17;33(29):3812-9. doi: 10.1038/onc.2013.357. Epub 2013 Sep 2.

Role of deoxycytidine kinase (dCK), thymidine kinase 2 (TK2), and deoxycytidine deaminase (dCDA) in the antitumor activity of gemcitabine (dFdC).

Adv Exp Med Biol. 1998;431:657-60. doi: 10.1007/978-1-4615-5381-6_127.

引用本文的文献

Comparative Molecular Docking of Apigenin and Luteolin versus Conventional Ligands for TP-53, pRb, APOBEC3H, and HPV-16 E6: Potential Clinical Applications in Preventing Gynecological Malignancies.

Curr Issues Mol Biol. 2024 Oct 3;46(10):11136-11155. doi: 10.3390/cimb46100661.

本文引用的文献

The cytidine deaminase APOBEC3C has unique sequence and genome feature preferences.

Genetics. 2024 Aug 7;227(4). doi: 10.1093/genetics/iyae092.

Cytidine deaminases APOBEC3C and APOBEC3D promote DNA replication stress resistance in pancreatic cancer cells.

Nat Cancer. 2024 Jun;5(6):895-915. doi: 10.1038/s43018-024-00742-z. Epub 2024 Mar 6.

APOBEC3A induces DNA gaps through PRIMPOL and confers gap-associated therapeutic vulnerability.

Sci Adv. 2024 Jan 19;10(3):eadk2771. doi: 10.1126/sciadv.adk2771.

The role of APOBEC3B in lung tumor evolution and targeted cancer therapy resistance.

Nat Genet. 2024 Jan;56(1):60-73. doi: 10.1038/s41588-023-01592-8. Epub 2023 Dec 4.

Human APOBEC3B promotes tumor development in vivo including signature mutations and metastases.

Cell Rep Med. 2023 Oct 17;4(10):101211. doi: 10.1016/j.xcrm.2023.101211. Epub 2023 Oct 4.

Therapy-induced APOBEC3A drives evolution of persistent cancer cells.

Nature. 2023 Aug;620(7973):393-401. doi: 10.1038/s41586-023-06303-1. Epub 2023 Jul 5.

Addressing the benefits of inhibiting APOBEC3-dependent mutagenesis in cancer.

Nat Genet. 2022 Nov;54(11):1599-1608. doi: 10.1038/s41588-022-01196-8. Epub 2022 Oct 24.

Mechanisms of APOBEC3 mutagenesis in human cancer cells.

Nature. 2022 Jul;607(7920):799-807. doi: 10.1038/s41586-022-04972-y. Epub 2022 Jul 20.

APOBEC3A drives deaminase domain-independent chromosomal instability to promote pancreatic cancer metastasis.

Nat Cancer. 2021 Dec;2(12):1338-1356. doi: 10.1038/s43018-021-00268-8. Epub 2021 Nov 18.

HMCES Maintains Replication Fork Progression and Prevents Double-Strand Breaks in Response to APOBEC Deamination and Abasic Site Formation.

Cell Rep. 2020 Jun 2;31(9):107705. doi: 10.1016/j.celrep.2020.107705.