Evidence map›Paper›PMID 39322638›Full record

ArticleOncogene2024

Characterisation of APOBEC3B-Mediated RNA editing in breast cancer cells reveals regulatory roles of NEAT1 and MALAT1 lncRNAs.

Chi Zhang, Yu-Jing Lu, Mei Wang, Bingjie Chen, Feifei Xiong, Costas Mitsopoulos, Olivia Rossanese, Xiuling Li, Paul A Clarke

Abstract read
In one paragraph

Article in Oncogene, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

8 citing papers in PubMed.

  1. Article
  2. Article
  3. HAMMER: Hairpin-based APOBEC3A-mediated mRNA editing reporter.bioRxiv : the preprint server for biology · 2026
    Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Chi Zhang *Centre for Cancer Drug Discovery, The Institute of Cancer Research, London, UK.
Yu-Jing Lu *Guangdong Medicine-Engineering Interdisciplinary Technology Research Centre, School of Biomedical and Pharmaceutical Sciences, Guangdong University of Technology, Guangzhou, China.ORCID 0000-0003-2494-843X
Mei WangShanghai Institute of Biological Products, Shanghai, China.
Bingjie ChenCentre for Cancer Drug Discovery, The Institute of Cancer Research, London, UK.
Feifei XiongShanghai Institute of Biological Products, Shanghai, China.
Costas MitsopoulosCentre for Cancer Drug Discovery, The Institute of Cancer Research, London, UK.
Olivia RossaneseCentre for Cancer Drug Discovery, The Institute of Cancer Research, London, UK.
Xiuling LiShanghai Institute of Biological Products, Shanghai, China. lixiuling@sinopharm.com.
Paul A ClarkeCentre for Cancer Drug Discovery, The Institute of Cancer Research, London, UK. paul.clarke@icr.ac.uk.ORCID 0000-0001-9342-1290

Funding

Science and Technology Commission of Shanghai Municipality (Shanghai Municipal Science and Technology Commission) 23S11901100
6 · The paper itself

Abstract

RNA editing is a crucial post-transcriptional process that influences gene expression and increases the diversity of the proteome as a result of amino acid substitution. Recently, the APOBEC3 family has emerged as a significant player in this mechanism, with APOBEC3A (A3A) having prominent roles in base editing during immune and stress responses. APOBEC3B (A3B), another family member, has gained attention for its potential role in generating genomic DNA mutations in breast cancer. In this study, we coupled an inducible expression cell model with a novel methodology for identifying differential variants in RNA (DVRs) to map A3B-mediated RNA editing sites in a breast cancer cell model. Our findings indicate that A3B engages in selective RNA editing including targeting NEAT1 and MALAT1 long non-coding RNAs that are often highly expressed in tumour cells. Notably, the binding of these RNAs sequesters A3B and suppresses global A3B activity against RNA and DNA. Release of A3B from NEAT1/MALAT1 resulted in increased A3B activity at the expense of A3A activity suggesting a regulatory feedback loop between the two family members. This research substantially advances our understanding of A3B's role in RNA editing, its mechanistic underpinnings, and its potential relevance in the pathogenesis of breast cancer.

Indexed as

Breast NeoplasmsCytidine DeaminaseMinor Histocompatibility AntigensRNA EditingRNA, Long NoncodingCell Line, TumorFemaleGene Expression Regulation, NeoplasticHumansAPOBEC3B protein, humanCytidine DeaminaseMALAT1 long non-coding RNA, humanMinor Histocompatibility AntigensNEAT1 long non-coding RNA, humanRNA, Long Noncoding

Identifiers

PMID39322638
PMCPMC11554567

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.