Evidence map›Paper›PMID 27043659›Full record

ArticleOncogenesis2016

Ultraconserved region-containing Transformer 2β4 controls senescence of colon cancer cells.

K Kajita, Y Kuwano, Y Satake, S Kano, K Kurokawa, Y Akaike, K Masuda, K Nishida, K Rokutan

Abstract read
In one paragraph

Article in Oncogenesis, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
–field-weighted citation impact
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

16 citing papers in PubMed.

  1. Ultra-Conserved Poison Exons Enable Rapid and Safe Splicing Factor Gene Expression Switches: A Hypothesis.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025
    Review
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. SPDL1 Is an Independent Predictor of Patient Outcome in Colorectal Cancer.International journal of molecular sciences · 2022
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. RNA Binding Proteins and Genome Integrity.International journal of molecular sciences · 2017
    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

9 authors.

K KajitaDepartment of Pathophysiology, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushima, Japan.
Y KuwanoDepartment of Pathophysiology, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushima, Japan.
Y SatakeDepartment of Pathophysiology, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushima, Japan.
S KanoDepartment of Pathophysiology, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushima, Japan.
K KurokawaDepartment of Pathophysiology, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushima, Japan.
Y AkaikeDepartment of Pathophysiology, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushima, Japan.
K MasudaDepartment of Pathophysiology, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushima, Japan.
K NishidaDepartment of Pathophysiology, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushima, Japan.
K RokutanDepartment of Pathophysiology, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushima, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ultraconserved regions (UCRs) are >200 bp genomic segments with perfect human-to-rodent sequence identity. Transcribed UCRs constitute a new category of noncoding RNAs whose functions remain poorly understood. The human transformer 2β (TRA2B) gene contains a 419-bp UCR spanning the 276-bp exon 2 and its neighboring introns. TRA2B exon 2 has premature stop codons, whereas an exon 2-containing splice variant (TRA2β4) was expressed preferentially in the nuclei of human colon cancer cells. TRA2β4 knockdown p53-independently stimulated CDKN1A transcription and increased p21, resulting in the appearance of senescent cells. Biotin pull-down and RNA immunoprecipitation assays revealed that TRA2β4 interacted with Sp1 through a Sp1-binding sequence (485-GGGG-488) in a stem-loop structure of exon 2. Mutation of this sequence (485-AAGG-488) disrupted the stem-loop structure, blocked the interaction with Sp1 and increased CDKN1A transcription. Overexpression of TRA2β4 significantly decreased CDKN1A mRNA levels and accelerated cell growth, but the introduction of the mutation in the Sp1-binding sequence completely canceled these effects. Taken together, TRA2β4 may sequester Sp1 from occupying promoters of target genes including CDKN1A, promoting cell growth by interrupting the senescence-related gene expression program. This novel function of TRA2β4 may uncover an oncogenic function of transcribed UCRs.

Identifiers

PMID27043659
PMCPMC4848834

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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.