Evidence map›Paper›PMID 31995627›Full record

ArticlePloS one2020

GLIPR1 expression is reduced in multiple myeloma but is not a tumour suppressor in mice.

Natasha Friend, Jacqueline E Noll, Khatora S Opperman, Kimberley C Clark, Krzysztof M Mrozik, Kate Vandyke, Duncan R Hewett, Andrew C W Zannettino

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.4field-weighted citation impact, top 39% 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

2 citing papers in PubMed, 4 citations in OpenAlex.

  1. CAP superfamily proteins in human: a new target for cancer therapy.Medical oncology (Northwood, London, England) · 2024
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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

8 authors at 1 institution in 1 country.

Natasha FriendAdelaide Medical School, Faculty of Health and Medical Sciences, University of Adelaide, Adelaide, Australia.ORCID 0000-0002-9191-0178
Jacqueline E NollAdelaide Medical School, Faculty of Health and Medical Sciences, University of Adelaide, Adelaide, Australia.
Khatora S OppermanAdelaide Medical School, Faculty of Health and Medical Sciences, University of Adelaide, Adelaide, Australia.
Kimberley C ClarkAdelaide Medical School, Faculty of Health and Medical Sciences, University of Adelaide, Adelaide, Australia.
Krzysztof M MrozikAdelaide Medical School, Faculty of Health and Medical Sciences, University of Adelaide, Adelaide, Australia.
Kate VandykeAdelaide Medical School, Faculty of Health and Medical Sciences, University of Adelaide, Adelaide, Australia.
Duncan R HewettAdelaide Medical School, Faculty of Health and Medical Sciences, University of Adelaide, Adelaide, Australia.
Andrew C W ZannettinoAdelaide Medical School, Faculty of Health and Medical Sciences, University of Adelaide, Adelaide, Australia.
South Australian Health and Medical Research Institute · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple myeloma, a plasma cell malignancy, is a genetically heterogeneous disease and the genetic factors that contribute to its development and progression remain to be fully elucidated. The tumour suppressor gene GLIPR1 has previously been shown to be deleted in approximately 10% of myeloma patients, to inhibit the development of plasma cell tumours in ageing mice and to have reduced expression levels in the plasma cells of patients with light-chain amyloidosis, a myeloma-related malignancy. Therefore, we hypothesised that GLIPR1 may have tumour suppressor activity in multiple myeloma. In this study, we demonstrate that plasma cell expression of GLIPR1 is reduced in the majority of myeloma patients and Glipr1 expression is lost in the 5TGM1 murine myeloma cell line. However, overexpression of GLIPR1 in a human myeloma cell line did not affect cell proliferation in vitro. Similarly, re-expression of Glipr1 in 5TGM1 cells did not significantly reduce their in vitro proliferation or in vivo growth in C57BL/KaLwRij mice. In addition, using CRISPR-Cas9 genome editing, we generated C57BL/Glipr1-/- mice and showed that loss of Glipr1 in vivo did not affect normal haematopoiesis or the development of monoclonal plasma cell expansions in these mice up to one year of age. Taken together, our results suggest that GLIPR1 is unlikely to be a potent tumour suppressor in multiple myeloma. However, it remains possible that the down-regulation of GLIPR1 may cooperate with other genetic lesions to promote the development of myeloma.

Indexed as

Down-RegulationAnimalsCell Line, TumorCell ProliferationGene EditingGene Expression Regulation, NeoplasticHumansIntercellular Signaling Peptides and ProteinsMaleMembrane ProteinsMiceMultiple MyelomaNeoplasm ProteinsNeoplasm TransplantationNerve Tissue ProteinsGLIPR1 protein, humanGlipr1 protein, mouseIntercellular Signaling Peptides and ProteinsMembrane ProteinsNeoplasm ProteinsNerve Tissue Proteins

Identifiers

PMID31995627
PMCPMC6988976
OpenAlexW3004008980

What OpenQuestion holds

Textmetadata
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.