Evidence map›Paper›PMID 28662214›Full record

ArticlePloS one2017

RBM10 promotes transformation-associated processes in small cell lung cancer and is directly regulated by RBM5.

Julie J Loiselle, Justin G Roy, Leslie C Sutherland

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

29 citing papers in PubMed, 44 citations in OpenAlex.

  1. Review
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  7. The therapeutic potential of RNA m(6)A in lung cancer.Cell communication and signaling : CCS · 2024
    Review
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  11. RNA-binding motif protein 10 inactivates c-Myc by partnering with ribosomal proteins uL18 and uL5.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
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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

3 authors at 2 institutions in 1 country.

Julie J LoiselleBiomolecular Sciences Program, Laurentian University, Sudbury, Ontario, Canada.ORCID http://orcid.org/0000-0003-3364-8447
Justin G RoyDepartment of Chemistry and Biochemistry, Laurentian University, Sudbury, Ontario, Canada.
Leslie C SutherlandBiomolecular Sciences Program, Laurentian University, Sudbury, Ontario, Canada.
Laurentian University · CAHealth Sciences North · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lung cancers are the leading cause of cancer-related deaths worldwide, with small cell lung cancer (SCLC) being the most aggressive type. At the time of diagnosis, SCLC has usually already metastasized, and an astonishing 95% of patients eventually succumb to the disease. This highlights the need for more effective SCLC screening and treatment options. Interestingly, the earliest and most frequent genetic alteration associated with lung cancers involves a lesion in the region to which the RNA binding protein RBM5 maps. We have recently shown that a decrease in RBM5 expression may be a key step in SCLC development, as RBM5 regulated many transformation-associated processes in SCLC cells. RBM5 is structurally and functionally similar to another RNA binding protein, RBM10. Both proteins have tumor-suppressor properties in a variety of cancer cell lines, and it has been suggested that RBM5 expression can influence RBM10. Due to their similarities, and the recent evidence that RBM10 is mutated in up to 21% of lung cancers, we hypothesized that RBM10 would share RBM5's tumor-suppressor properties in SCLC. Using transcriptome analysis and functional assays, we show, however, that RBM10's function was opposite to what we hypothesized; in the endogenously RBM5-null GLC20 SCLC cell line, RBM10 actually promoted cell proliferation and other transformation-associated processes. Using RNA immunoprecipitation followed by next generation sequencing (RIP-Seq) and Western blotting, we demonstrate that RBM5 post-transcriptionally regulated RBM10 expression via direct interaction with specific RBM10 splice variants. We propose a working model describing the impact of this interaction on cellular processes. Our results provide evidence that RBM10 expression, in RBM5-null tumors, may contribute to tumor growth and metastasis. Measurement of both RBM10 and RBM5 expression in clinical samples may therefore hold prognostic and/or potentially predictive value.

Indexed as

Cell Transformation, NeoplasticCell Cycle ProteinsCell Line, TumorCell ProliferationDNA-Binding ProteinsDNA, ComplementaryHumansLung NeoplasmsMutationRNA-Binding ProteinsSequence Analysis, RNASmall Cell Lung CarcinomaTumor Suppressor ProteinsCell Cycle ProteinsDNA-Binding ProteinsDNA, ComplementaryRBM10 protein, humanRBM5 protein, humanRNA-Binding ProteinsTumor Suppressor Proteins

Identifiers

PMID28662214
PMCPMC5491171
OpenAlexW2724508033

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.