APOBEC3B is preferentially expressed at the G2/M phase of cell cycle

Hirabayashi, Shigeki; Shirakawa, Kotaro; Horisawa, Yoshihito; Matsumoto, Tadahiko; Matsui, Hiroyuki; Yamazaki, Hiroaki; Sarca, Anamaria Daniela; Kazuma, Yasuhiro; Konishi, Yoshinobu; Takeuchi, Suguru; Stanford, Emani; Kawaji, Hideya; Murakawa, Yuji; Takaori‐Kondo, Akifumi

doi:10.1016/j.bbrc.2021.02.008

Cited by 14 publications

(15 citation statements)

References 28 publications

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“…Gene ontology analysis of the A3B-dependent R-loop interactome demonstrated the enrichment of proteins involved in regulating the cell cycle and cellular response to stress (Fig. 1f), consistent with previously established functions of A3B 27 . These data indicated that A3B might maintain the R-loop interactome to modulate cell cycle, stress response or gene transcription.…”

Section: Resultssupporting

confidence: 87%

APOBEC3B coordinates R-loop to promote replication stress and sensitize cancer cells to ATR/Chk1 inhibitors

Zong

Zhang

Gao

et al. 2023

Preprint

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The cytidine deaminase, Apolipoprotein B mRNA editing enzyme catalytic subunit 3B (APOBEC3B, herein termed A3B), is a critical mutation driver that induces genomic instability in cancer by catalyzing cytosine-to-thymine (C-to-T) conversion and promoting replication stress. However, the detailed function of A3B in replication stress is not fully determined and it is not known whether the mechanism of A3B action can be exploited for cancer therapy. Here, we conducted an immunoprecipitation-mass spectrometry (IP-MS) study and identified A3B to be a novel binding component of R-loops, which are RNA:DNA hybrid structures. Mechanistically, overexpression of A3B exacerbated replication stress by promoting R-loop formation and altering the distribution of R-loops in the genome. This was rescued by the R-loop gatekeeper, Ribonuclease H1 (RNASEH1). In addition, a high level of A3B conferred sensitivity to ATR/Chk1 inhibitors in melanoma cells, which was dependent on R-loop status. Together, our results provide novel insights into the mechanistic link between A3B and R-loops in the promotion of replication stress in cancer. This will inform the development of markers to predict the response of patients to ATR/Chk1 inhibitors.

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Section: Resultssupporting

confidence: 87%

APOBEC3B coordinates R-loop to promote replication stress and sensitize cancer cells to ATR/Chk1 inhibitors

Zong

Zhang

Gao

et al. 2023

Preprint

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“… 109 , 110 Moreover, single‐cell RNA sequencing (scRNA‐seq) provides a novel perspective for exploring the functions of circRNA at single‐cell resolution to understand their cell‐specific regulation as well as cell cycle regulation. 111 , 112 A recent study reported a new data analysis technique for circRNA – CIRI‐long – that uses nanopore long reads and enables unbiased reconstruction of full‐length circRNA sequences. 113 CircRNAs exert proper biological functions through dynamically regulated biogenesis and degradation; however, the mechanism of their degradation remains largely unknown.…”

Section: Potential Diagnostic and Therapeutic Applications Of Circrnasmentioning

confidence: 99%

Circular RNAs in cell cycle regulation: Mechanisms to clinical significance

Xiao

et al. 2021

Cell Proliferation

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Circular RNAs (circRNAs), a type of non‐coding RNA, are single‐stranded circularized molecules characterized by high abundance, evolutionary conservation and cell development‐ and tissue‐specific expression. A large body of studies has found that circRNAs exert a wide variety of functions in diverse biological processes, including cell cycle. The cell cycle is controlled by the coordinated activation and deactivation of cell cycle regulators. CircRNAs exert mutifunctional roles by regulating gene expression via various mechanisms. However, the functional relevance of circRNAs and cell cycle regulation largely remains to be elucidated. Herein, we briefly describe the biogenesis and mechanistic models of circRNAs and summarize their functions and mechanisms in the regulation of critical cell cycle modulators, including cyclins, cyclin‐dependent kinases and cyclin‐dependent kinase inhibitors. Moreover, we highlight the participation of circRNAs in cell cycle‐related signalling pathways and the clinical value of circRNAs as promising biomarkers or therapeutic targets in diseases related to cell cycle disorder.

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“…Second, viral genome amplification occurs in cells that are arrested in a G2like state via the action of viral proteins including E1^E4 [31,32]. Both APOBEC3A and APOBEC3B are preferentially expressed during G2 [33][34][35], both are induced upon differentiation of HPV-infected cells in vitro [36] and APOBEC3A is also expressed in the midlayers of normal oropharyngeal epithelium [37]. Deamination of the viral genome during G2 could potentially explain the lack of C>G transversions seen by Zhu and colleagues, since distinct mutational outcomes have been observed following translesion synthesis (the process primarily responsible for mutagenesis following cytosine deamination) in G2 versus S-phase in mammalian cells [38].…”

Section: Is Viral Genome Editing Associated With Vegetative Hpv Genom...mentioning

confidence: 99%

Accumulation of host cell genetic errors following high-risk HPV infection

Fenton

2021

Current Opinion in Virology

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APOBEC3B is preferentially expressed at the G2/M phase of cell cycle

Cited by 14 publications

References 28 publications

APOBEC3B coordinates R-loop to promote replication stress and sensitize cancer cells to ATR/Chk1 inhibitors

APOBEC3B coordinates R-loop to promote replication stress and sensitize cancer cells to ATR/Chk1 inhibitors

Circular RNAs in cell cycle regulation: Mechanisms to clinical significance

Accumulation of host cell genetic errors following high-risk HPV infection

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