Evidence map›Paper›PMID 23113893›Full record

ArticleCancer science2013

SAP155-mediated c-myc suppressor far-upstream element-binding protein-interacting repressor splicing variants are activated in colon cancer tissues.

Toshiko Kajiwara, Kazuyuki Matsushita, Sakae Itoga, Mai Tamura, Nobuko Tanaka, Takeshi Tomonaga, Hisahiro Matsubara, Hideaki Shimada, Yasuaki Habara, Masafumi Matsuo and 1 more

Open access · greenAbstract read
In one paragraph

Article in Cancer science, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

23 citing papers in PubMed, 42 citations in OpenAlex.

  1. International journal of molecular sciences · 2026
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  11. Frontiers in oncology · 2020
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  15. Oncotarget · 2017
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  16. Alternative Splicing of EZH2 pre-mRNA by SF3B3 Contributes to the Tumorigenic Potential of Renal Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2017
    Article
  17. 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

11 authors at 4 institutions in 1 country.

Toshiko KajiwaraDepartment of Molecular Diagnosis, Chiba University Graduate School of Medicine, Chiba, Japan.
Kazuyuki Matsushita
Sakae Itoga
Mai Tamura
Nobuko Tanaka
Takeshi Tomonaga
Hisahiro Matsubara
Hideaki Shimada
Yasuaki Habara
Masafumi Matsuo
Fumio Nomura
Chiba University · JPKobe University · JPNational Institute of Biomedical Innovation, Health and Nutrition · JPToho University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The c-myc transcriptional suppressor, far-upstream element (FUSE)-binding protein (FBP)-interacting repressor (FIR), is alternatively spliced in colorectal cancer tissue (Matsushita et al., Cancer Res 2006). Recently, the knockdown of SAP155 pre-mRNA-splicing factor, a subunit of SF3b, was reported to disturb FIR pre-mRNA splicing and yield FIRΔexon2, an exon 2-spliced variant of FIR, which lacks c-myc repression activity. In the present study, novel splicing variants of FIR, Δ3 and Δ4, were also generated by SAP155 siRNA, and these variants were found to be activated in human colorectal cancer tissue. Furthermore, the expression levels of FIR variant mRNA were examined in the peripheral blood of colorectal cancer patients and healthy volunteers to assess its potency for tumor detection. As expected, circulating FIR variant mRNA in the peripheral blood of cancer patients were significantly overexpressed compared to that in healthy volunteers. In particular, the area under the receiving operating characteristic curve of FIR, FIRΔexon2 or FIRΔexon2/FIR, was greater than those of conventional carcinoembryonic antigen or carbohydrate antigen 19-9. In addition, FIRΔexon2 or FIR mRNA expression in the peripheral blood was significantly reduced after operative removal of colorectal tumors. Thus, circulating FIR and FIRΔexon2 mRNA are potential novel screening markers for colorectal cancer testing with conventional carcinoembryonic antigen and or carbohydrate antigen 19-9. Taken together, our results indicate that overexpression of FIR and its splicing variants in colorectal cancer directs feed-forward or addicted circuit c-myc transcriptional activation. Clinical implications for colorectal cancers of novel FIR splicing variants are also discussed in the present paper.

Indexed as

Alternative SplicingAnimalsAntigens, Tumor-Associated, CarbohydrateBiomarkers, TumorCell Line, TumorChlorocebus aethiopsColonic NeoplasmsCOS CellsExonsGenes, Tumor SuppressorGuanine Nucleotide Exchange FactorsHCT116 CellsHeLa CellsHumansPhosphoproteinsProtein IsoformsAntigens, Tumor-Associated, CarbohydrateBiomarkers, Tumorcarbohydrate antigen 199, humanFARP2 protein, humanGuanine Nucleotide Exchange FactorsPhosphoproteinsProtein IsoformsProto-Oncogene Proteins c-mycRho Guanine Nucleotide Exchange FactorsRibonucleoprotein, U2 Small NuclearRNA, MessengerRNA PrecursorsRNA, Small InterferingRNA Splicing FactorsSF3B1 protein, human

Identifiers

PMID23113893
PMCPMC7657139
OpenAlexW1982496394

What OpenQuestion holds

Textmetadata
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Registered trials

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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.