Evidence map›Paper›PMID 26367347›Full record

ArticleRNA biology2015

SRSF3 and hnRNP H1 regulate a splicing hotspot of HER2 in breast cancer cells.

Hannah Gautrey, Claire Jackson, Anna-Lena Dittrich, David Browell, Thomas Lennard, Alison Tyson-Capper

Open access · bronzeAbstract read
In one paragraph

Article in RNA biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

62 citing papers in PubMed, 76 citations in OpenAlex.

  1. SRSF3 plays a key role in liver cancer sex disparity by facilitating hepatocyte expression of ERα and FOXA.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  18. The RNA-binding proteins hnRNP H and F regulate splicing of a MYC-dependent HRAS exon in prostate cancer cells.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
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2 more citing papers are in PubMed but not listed here.

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

6 authors at 3 institutions in 1 country.

Hannah Gautreya Institute of Cellular Medicine; Faculty of Medical Sciences; Newcastle University ; Newcastle upon Tyne , UK.
Claire Jacksona Institute of Cellular Medicine; Faculty of Medical Sciences; Newcastle University ; Newcastle upon Tyne , UK.
Anna-Lena Dittricha Institute of Cellular Medicine; Faculty of Medical Sciences; Newcastle University ; Newcastle upon Tyne , UK.
David Browellb Queen Elizabeth Hospital, Gateshead ; Tyne and Wear , UK.
Thomas Lennardc Northern Institute for Cancer Research; Faculty of Medical Sciences; Newcastle University ; Newcastle upon Tyne , UK.
Alison Tyson-Cappera Institute of Cellular Medicine; Faculty of Medical Sciences; Newcastle University ; Newcastle upon Tyne , UK.
Newcastle University · GBCumbria Northumberland Tyne and Wear NHS Foundation Trust · GBNewcastle upon Tyne Hospital · GB

Funding

Medical Research Council MC_PC_14101
6 · The paper itself

Abstract

Overexpression of the oncogene HER2 occurs in 20-30% of invasive breast cancer and is associated with poor prognosis. A number of different splice variants of HER2 have been identified which produce functionally different proteins. Previously these splice variants have been investigated separately, but in the present study we collectively look at the expression and regulation of a group of HER2 splice variants produced by a splicing hotspot. Initial investigation in a cohort of tumor samples showed large variations in HER2 variant expression between patient samples. RNA interference studies identified 2 splicing factors involved in the regulation of splicing within this region, hnRNP H1 and SRSF3. siRNA targeting hnRNP H1 increases levels of X5 and the oncogenic variant Δ16HER2. Furthermore RNA chromatography assays demonstrated binding of hnRNP H1 to RNA in this region. Additionally the proto-oncogene SRSF3 was also identified as an important regulator of splicing with SRSF3 knockdown resulting in changes in all the splice variants located at the hotspot. Most notably knockdown of SRSF3 resulted in a switch from the oncogenic Δ16HER2 to p100 which inhibits cell proliferation. Binding of SRSF3 to RNA within this region was also demonstrated by RNA chromatography and more specifically 2 SRSF3 binding sites were identified within exon 15. SRSF3 and hnRNP H1 are the first splicing factors identified which regulate the production of these functionally distinct HER2 splice variants and therefore maybe important for the regulation of HER2 signaling.

Indexed as

Alternative SplicingBinding SitesBreast NeoplasmsCell Line, TumorCell ProliferationErb-b2 Receptor Tyrosine KinasesFemaleGene Expression Regulation, NeoplasticGene Knockdown TechniquesHeterogeneous-Nuclear Ribonucleoprotein Group F-HHumansProto-Oncogene MasRNA-Binding ProteinsSerine-Arginine Splicing FactorsERBB2 protein, humanErb-b2 Receptor Tyrosine KinasesHeterogeneous-Nuclear Ribonucleoprotein Group F-HMAS1 protein, humanProto-Oncogene MasRNA-Binding ProteinsSerine-Arginine Splicing FactorsSRSF3 protein, humanbreast cancerHER2hnRNP H1RNA binding proteinssplice variantsSRSF3

Identifiers

PMID26367347
PMCPMC4829299
OpenAlexW2118842644

What OpenQuestion holds

Textmetadata
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.