Evidence map›Paper›PMID 33625522›Full record

ReviewCellular and molecular life sciences : CMLS2021

Evolution, structure and emerging roles of C1ORF112 in DNA replication, DNA damage responses, and cancer.

Jacob Edogbanya, Daniela Tejada-Martinez, Nigel J Jones, Amit Jaiswal, Sarah Bell, Rui Cordeiro, Sipko van Dam, Daniel J Rigden, João Pedro de Magalhães

Open access · hybridAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

16 citing papers in PubMed, 20 citations in OpenAlex.

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  4. C1orf112 promotes breast cancer growth by modulating the cell cycle.Frontiers in bioengineering and biotechnology · 2026
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  16. Pan-Cancer Analysis IdentifiedFrontiers in molecular biosciences · 2021
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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 6 countries.

Jacob Edogbanya *Integrative Genomics of Ageing Group, Institute of Ageing and Chronic Disease, University of Liverpool, Liverpool, L7 8TX, UK.
Daniela Tejada-Martinez *Integrative Genomics of Ageing Group, Institute of Ageing and Chronic Disease, University of Liverpool, Liverpool, L7 8TX, UK.
Nigel J Jones *Institute of Systems, Molecular and Integrative Biology, University of Liverpool, Liverpool, L69 7ZB, UK.
Amit Jaiswal *Institute of Aging Research, School of Medicine, Hangzhou Normal University, Hangzhou, China.ORCID http://orcid.org/0000-0002-4778-5955
Sarah BellInstitute of Systems, Molecular and Integrative Biology, University of Liverpool, Liverpool, L69 7ZB, UK.
Rui CordeiroIntegrative Genomics of Ageing Group, Institute of Ageing and Chronic Disease, University of Liverpool, Liverpool, L7 8TX, UK.
Sipko van DamDepartment of Endocrinology, University of Groningen, University Medical Center Groningen, Hanzeplein 1, 9713 GZ, Groningen, The Netherlands.
Daniel J RigdenInstitute of Systems, Molecular and Integrative Biology, University of Liverpool, Liverpool, L69 7ZB, UK.
João Pedro de MagalhãesIntegrative Genomics of Ageing Group, Institute of Ageing and Chronic Disease, University of Liverpool, Liverpool, L7 8TX, UK. jp@senescence.info.ORCID http://orcid.org/0000-0002-6363-2465
University of Liverpool · GBHangzhou Normal University · CNUniversity Medical Center Groningen · NL

Funding

Biotechnology and Biological Sciences Research Council BB/R014949/1Wellcome TrustWellcome Trust 208375/Z/17/Z
6 · The paper itself

Abstract

The C1ORF112 gene initially drew attention when it was found to be strongly co-expressed with several genes previously associated with cancer and implicated in DNA repair and cell cycle regulation, such as RAD51 and the BRCA genes. The molecular functions of C1ORF112 remain poorly understood, yet several studies have uncovered clues as to its potential functions. Here, we review the current knowledge on C1ORF112 biology, its evolutionary history, possible functions, and its potential relevance to cancer. C1ORF112 is conserved throughout eukaryotes, from plants to humans, and is very highly conserved in primates. Protein models suggest that C1ORF112 is an alpha-helical protein. Interestingly, homozygous knockout mice are not viable, suggesting an essential role for C1ORF112 in mammalian development. Gene expression data show that, among human tissues, C1ORF112 is highly expressed in the testes and overexpressed in various cancers when compared to healthy tissues. C1ORF112 has also been shown to have altered levels of expression in some tumours with mutant TP53. Recent screens associate C1ORF112 with DNA replication and reveal possible links to DNA damage repair pathways, including the Fanconi anaemia pathway and homologous recombination. These insights provide important avenues for future research in our efforts to understand the functions and potential disease relevance of C1ORF112.

Indexed as

Biological EvolutionDNA DamageDNA RepairDNA ReplicationAnimalsHumansMaleNeoplasmsOpen Reading FramesProtein Interaction MapsTestisBC055324DNA repairFanconi anaemiaOncogeneTumour

Identifiers

PMID33625522
PMCPMC8164572
OpenAlexW3130017103

What OpenQuestion holds

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LicenceCC BY
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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.