Evidence map›Paper›PMID 34363951›Full record

ArticleCellular signalling2021

hMOB2 deficiency impairs homologous recombination-mediated DNA repair and sensitises cancer cells to PARP inhibitors.

Ramazan Gundogdu, M Kadir Erdogan, Angeliki Ditsiou, Victoria Spanswick, Juan Jose Garcia-Gomez, John A Hartley, Fumiko Esashi, Alexander Hergovich, Valenti Gomez

Open access · hybridAbstract read
In one paragraph

Article in Cellular signalling, 2021. 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
0.6field-weighted citation impact, top 33% of its field
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, 16 citations in OpenAlex.

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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 at 3 institutions in 2 countries.

Ramazan GundogduDepartment of Biology, Bingol University, Bingol 12000, Turkey; UCL Cancer Institute, University College London, London WC1E 6DD, UK. Electronic address: rgundogdu@bingol.edu.tr.
M Kadir ErdoganDepartment of Biology, Bingol University, Bingol 12000, Turkey.
Angeliki DitsiouDepartment of Biochemistry and Biomedicine, University of Sussex, Brighton BN1 9QG, UK; UCL Cancer Institute, University College London, London WC1E 6DD, UK.
Victoria SpanswickUCL Cancer Institute, University College London, London WC1E 6DD, UK.
Juan Jose Garcia-GomezUCL Cancer Institute, University College London, London WC1E 6DD, UK.
John A HartleyUCL Cancer Institute, University College London, London WC1E 6DD, UK.
Fumiko EsashiSir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, UK.
Alexander HergovichUCL Cancer Institute, University College London, London WC1E 6DD, UK; Evotec France, Toulouse 31100, France.
Valenti GomezUCL Cancer Institute, University College London, London WC1E 6DD, UK. Electronic address: valenti.gomezma@gmail.com.
University College London · GBBingöl University · TRUniversity of Oxford · GB

Funding

Biotechnology and Biological Sciences Research Council BB/I021248/1Cancer Research UK C7893/A26233Wellcome TrustWellcome Trust 090090/Z/09/Z
6 · The paper itself

Abstract

Monopolar spindle-one binder (MOBs) proteins are evolutionarily conserved and contribute to various cellular signalling pathways. Recently, we reported that hMOB2 functions in preventing the accumulation of endogenous DNA damage and a subsequent p53/p21-dependent G1/S cell cycle arrest in untransformed cells. However, the question of how hMOB2 protects cells from endogenous DNA damage accumulation remained enigmatic. Here, we uncover hMOB2 as a regulator of double-strand break (DSB) repair by homologous recombination (HR). hMOB2 supports the phosphorylation and accumulation of the RAD51 recombinase on resected single-strand DNA (ssDNA) overhangs. Physiologically, hMOB2 expression supports cancer cell survival in response to DSB-inducing anti-cancer compounds. Specifically, loss of hMOB2 renders ovarian and other cancer cells more vulnerable to FDA-approved PARP inhibitors. Reduced MOB2 expression correlates with increased overall survival in patients suffering from ovarian carcinoma. Taken together, our findings suggest that hMOB2 expression may serve as a candidate stratification biomarker of patients for HR-deficiency targeted cancer therapies, such as PARP inhibitor treatments.

Indexed as

NeoplasmsPoly(ADP-ribose) Polymerase InhibitorsCell Line, TumorDNA DamageDNA RepairHomologous RecombinationHumansPoly(ADP-ribose) Polymerase InhibitorsDNA damage response signallingHomologous recombination DNA repairMps one binder 2 (MOB2)Personalised PARP inhibitor treatments

Identifiers

PMID34363951
PMCPMC8514680
OpenAlexW3190326542

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.