Evidence map›Paper›PMID 27555542›Full record

ArticleMolecular oncology2016

A large-scale analysis of alternative splicing reveals a key role of QKI in lung cancer.

Fernando J de Miguel, María J Pajares, Elena Martínez-Terroba, Daniel Ajona, Xabier Morales, Ravi D Sharma, Francisco J Pardo, Ana Rouzaut, Angel Rubio, Luis M Montuenga and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Molecular oncology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

56 citing papers in PubMed, 74 citations in OpenAlex.

  1. Article
  2. Review
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  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Qki5 safeguards spinal motor neuron function by defining the motor neuron-specific transcriptome via pre-mRNA processing.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  13. Article
  14. Review
  15. Review
  16. Expression profiling of luminal B breast tumor in Indian women.Journal of cancer research and clinical oncology · 2023
    Article
  17. Article
  18. The role of alternative splicing in lung cancer.Cancer chemotherapy and pharmacology · 2023
    Review
  19. Article
  20. Role of the RNA-binding protein family in gynecologic cancers.American journal of cancer research · 2023
    Review
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

11 authors at 4 institutions in 1 country.

Fernando J de MiguelProgram in Solid Tumors and Biomarkers, CIMA, 31008 Pamplona, Spain; Department of Biochemistry and Genetics, School of Science, University of Navarra, 31008 Pamplona, Spain.
María J PajaresProgram in Solid Tumors and Biomarkers, CIMA, 31008 Pamplona, Spain; Department of Histology and Pathology, School of Medicine, University of Navarra, 31008 Pamplona, Spain; Navarra's Health Research Institute (IDISNA), 31008 Pamplona, Spain.
Elena Martínez-TerrobaProgram in Solid Tumors and Biomarkers, CIMA, 31008 Pamplona, Spain; Department of Histology and Pathology, School of Medicine, University of Navarra, 31008 Pamplona, Spain.
Daniel AjonaProgram in Solid Tumors and Biomarkers, CIMA, 31008 Pamplona, Spain; Department of Biochemistry and Genetics, School of Science, University of Navarra, 31008 Pamplona, Spain; Navarra's Health Research Institute (IDISNA), 31008 Pamplona, Spain.
Xabier MoralesProgram in Immunology and Immunotherapy, CIMA, 31008 Pamplona, Spain.
Ravi D SharmaGroup of Bioinformatics, CEIT and TECNUN, University of Navarra, 20018 San Sebastian, Spain.
Francisco J PardoDepartment of Pathology, Clinica Universidad de Navarra, 31080 Pamplona, Spain.
Ana RouzautDepartment of Biochemistry and Genetics, School of Science, University of Navarra, 31008 Pamplona, Spain; Navarra's Health Research Institute (IDISNA), 31008 Pamplona, Spain; Program in Immunology and Immunotherapy, CIMA, 31008 Pamplona, Spain.
Angel RubioGroup of Bioinformatics, CEIT and TECNUN, University of Navarra, 20018 San Sebastian, Spain.
Luis M MontuengaProgram in Solid Tumors and Biomarkers, CIMA, 31008 Pamplona, Spain; Department of Histology and Pathology, School of Medicine, University of Navarra, 31008 Pamplona, Spain; Navarra's Health Research Institute (IDISNA), 31008 Pamplona, Spain. Electronic address: lmontuenga@unav.es.
Ruben PioProgram in Solid Tumors and Biomarkers, CIMA, 31008 Pamplona, Spain; Department of Biochemistry and Genetics, School of Science, University of Navarra, 31008 Pamplona, Spain; Navarra's Health Research Institute (IDISNA), 31008 Pamplona, Spain. Electronic address: rpio@unav.es.
Universidad de Navarra · ESNavarre Institute of Health Research · ESCentro de Estudios e Investigaciones Técnicas de Gipuzkoa · ESClinica Universidad de Navarra · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Increasing interest has been devoted in recent years to the understanding of alternative splicing in cancer. In this study, we performed a genome-wide analysis to identify cancer-associated splice variants in non-small cell lung cancer. We discovered and validated novel differences in the splicing of genes known to be relevant to lung cancer biology, such as NFIB, ENAH or SPAG9. Gene enrichment analyses revealed an important contribution of alternative splicing to cancer-related molecular functions, especially those involved in cytoskeletal dynamics. Interestingly, a substantial fraction of the altered genes found in our analysis were targets of the protein quaking (QKI), pointing to this factor as one of the most relevant regulators of alternative splicing in non-small cell lung cancer. We also found that ESYT2, one of the QKI targets, is involved in cytoskeletal organization. ESYT2-short variant inhibition in lung cancer cells resulted in a cortical distribution of actin whereas inhibition of the long variant caused an increase of endocytosis, suggesting that the cancer-associated splicing pattern of ESYT2 has a profound impact in the biology of cancer cells. Finally, we show that low nuclear QKI expression in non-small cell lung cancer is an independent prognostic factor for disease-free survival (HR = 2.47; 95% CI = 1.11-5.46, P = 0.026). In conclusion, we identified several splicing variants with functional relevance in lung cancer largely regulated by the splicing factor QKI, a tumor suppressor associated with prognosis in lung cancer.

Indexed as

Alternative SplicingCarcinoma, Non-Small-Cell LungClathrinCytoskeletonDown-RegulationExonsGene Expression Regulation, NeoplasticHumansLung NeoplasmsPrognosisRNA-Binding ProteinsSynaptotagminsClathrinQKI protein, humanRNA-Binding ProteinsSynaptotagminsAlternative splicingESYT2Non-small cell lung cancerQKI

Identifiers

PMID27555542
PMCPMC5423218
OpenAlexW2502573483

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.