دورية أكاديمية
أعرض في EDS

Adaptive use of error-prone DNA polymerases provides flexibility in genome replication during tumorigenesis.

التفاصيل البيبلوغرافية
العنوان: Adaptive use of error-prone DNA polymerases provides flexibility in genome replication during tumorigenesis.
المؤلفون: Bainbridge LJ; Cancer Genome Dynamics Project, Cancer Institute, Japanese Foundation for Cancer Research, Tokyo, Japan., Daigaku Y; Cancer Genome Dynamics Project, Cancer Institute, Japanese Foundation for Cancer Research, Tokyo, Japan.
المصدر: Cancer science [Cancer Sci] 2024 Jul; Vol. 115 (7), pp. 2125-2137. Date of Electronic Publication: 2024 Apr 23.
نوع المنشور: Journal Article; Review
اللغة: English
بيانات الدورية: Publisher: Wiley Publishing on behalf of the Japanese Cancer Association Country of Publication: England NLM ID: 101168776 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1349-7006 (Electronic) Linking ISSN: 13479032 NLM ISO Abbreviation: Cancer Sci Subsets: MEDLINE
أسماء مطبوعة: Publication: 2005- : Oxford : Wiley Publishing on behalf of the Japanese Cancer Association
Original Publication: Tokyo : Japanese Cancer Association, c2003-
مواضيع طبية MeSH: DNA Replication* , DNA-Directed DNA Polymerase*/metabolism , DNA-Directed DNA Polymerase*/genetics , Carcinogenesis*/genetics , Neoplasms*/genetics , Neoplasms*/pathology, Humans ; Animals ; Proliferating Cell Nuclear Antigen/metabolism ; Proliferating Cell Nuclear Antigen/genetics ; Ubiquitination ; Mutagenesis ; DNA Repair/genetics
مستخلص: Human cells possess many different polymerase enzymes, which collaborate in conducting DNA replication and genome maintenance to ensure faithful duplication of genetic material. Each polymerase performs a specialized role, together providing a balance of accuracy and flexibility to the replication process. Perturbed replication increases the requirement for flexibility to ensure duplication of the entire genome. Flexibility is provided via the use of error-prone polymerases, which maintain the progression of challenged DNA replication at the expense of mutagenesis, an enabling characteristic of cancer. This review describes our recent understanding of mechanisms that alter the usage of polymerases during tumorigenesis and examines the implications of this for cell survival and tumor progression. Although expression levels of polymerases are often misregulated in cancers, this does not necessarily alter polymerase usage since an additional regulatory step may govern the use of these enzymes. We therefore also examine how the regulatory mechanisms of DNA polymerases, such as Rad18-mediated PCNA ubiquitylation, may impact the functionalization of error-prone polymerases to tolerate oncogene-induced replication stress. Crucially, it is becoming increasingly evident that cancer cells utilize error-prone polymerases to sustain ongoing replication in response to oncogenic mutations which inactivate key DNA replication and repair pathways, such as BRCA deficiency. This accelerates mutagenesis and confers chemoresistance, but also presents a dependency that can potentially be exploited by therapeutics.
(© 2024 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association.)
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معلومات مُعتمدة: Yamada Science Foundation; JP23H02463 Japan Society for the Promotion of Science; Takeda Science Foundation; JPMJFR204X Fusion Oriented REsearch for disruptive Science and Technology; Naito Foundation
فهرسة مساهمة: Keywords: DNA polymerase; DNA replication; PCNA ubiquitylation; mutagenesis; replication stress
المشرفين على المادة: EC 2.7.7.7 (DNA-Directed DNA Polymerase)
0 (Proliferating Cell Nuclear Antigen)
تواريخ الأحداث: Date Created: 20240423 Date Completed: 20240712 Latest Revision: 20240717
رمز التحديث: 20240717
مُعرف محوري في PubMed: PMC11247608
DOI: 10.1111/cas.16188
PMID: 38651239
قاعدة البيانات: MEDLINE
الوصف
تدمد:1349-7006
DOI:10.1111/cas.16188