Evidence map›Paper›PMID 26273626›Full record

ReviewBioMed research international2015

SAM68: Signal Transduction and RNA Metabolism in Human Cancer.

Paola Frisone, Davide Pradella, Anna Di Matteo, Elisa Belloni, Claudia Ghigna, Maria Paola Paronetto

Open access · hybridAbstract readReview
In one paragraph

Review in BioMed research international, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

68 citing papers in PubMed, 116 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Review
  9. Role of Sam68 in different types of cancer (Review).International journal of molecular medicine · 2025
    Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Role of Sam68 as an adaptor protein in inflammatory signaling.Cellular and molecular life sciences : CMLS · 2024
    Review
  17. RNA-binding proteins in bone pathophysiology.Frontiers in cell and developmental biology · 2024
    Review
  18. Expression ofMolecular therapy. Nucleic acids · 2023
    Article
  19. Article
  20. Review

8 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.

Paola FrisoneLaboratory of Cellular and Molecular Neurobiology, Santa Lucia Foundation, 00143 Rome, Italy.
Davide PradellaInstitute of Molecular Genetics-National Research Council (IGM-CNR), 27100 Pavia, Italy.
Anna Di MatteoInstitute of Molecular Genetics-National Research Council (IGM-CNR), 27100 Pavia, Italy.
Elisa BelloniInstitute of Molecular Genetics-National Research Council (IGM-CNR), 27100 Pavia, Italy.
Claudia GhignaInstitute of Molecular Genetics-National Research Council (IGM-CNR), 27100 Pavia, Italy.
Maria Paola ParonettoLaboratory of Cellular and Molecular Neurobiology, Santa Lucia Foundation, 00143 Rome, Italy ; University of Rome "Foro Italico", Piazza Lauro de Bosis 15, 00135 Rome, Italy.
National Research Council · ITFondazione Santa Lucia · ITForo Italico University of Rome · IT

Funding

Worldwide Cancer Research 14-0333
6 · The paper itself

Abstract

Alterations in expression and/or activity of splicing factors as well as mutations in cis-acting splicing regulatory sequences contribute to cancer phenotypes. Genome-wide studies have revealed more than 15,000 tumor-associated splice variants derived from genes involved in almost every aspect of cancer cell biology, including proliferation, differentiation, cell cycle control, metabolism, apoptosis, motility, invasion, and angiogenesis. In the past decades, several RNA binding proteins (RBPs) have been implicated in tumorigenesis. SAM68 (SRC associated in mitosis of 68 kDa) belongs to the STAR (signal transduction and activation of RNA metabolism) family of RBPs. SAM68 is involved in several steps of mRNA metabolism, from transcription to alternative splicing and then to nuclear export. Moreover, SAM68 participates in signaling pathways associated with cell response to stimuli, cell cycle transitions, and viral infections. Recent evidence has linked this RBP to the onset and progression of different tumors, highlighting misregulation of SAM68-regulated splicing events as a key step in neoplastic transformation and tumor progression. Here we review recent studies on the role of SAM68 in splicing regulation and we discuss its contribution to aberrant pre-mRNA processing in cancer.

Indexed as

Signal TransductionAdaptor Proteins, Signal TransducingBiomarkers, TumorDNA-Binding ProteinsHumansNeoplasmsPolymorphism, Single NucleotideRNA-Binding ProteinsRNA, NeoplasmRNA SplicingAdaptor Proteins, Signal TransducingBiomarkers, TumorDNA-Binding ProteinsKHDRBS1 protein, humanRNA-Binding ProteinsRNA, Neoplasm

Identifiers

PMID26273626
PMCPMC4529925
OpenAlexW1534005970

What OpenQuestion holds

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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.