Evidence map›Paper›PMID 26477307›Full record

ArticleOncogene2016

Positive regulation of β-catenin-PROX1 signaling axis by DBC1 in colon cancer progression.

E J Yu, S-H Kim, H J Kim, K Heo, C-Y Ou, M R Stallcup, J H Kim

Open access · bronzeAbstract read
In one paragraph

Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 17% 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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Translational lung cancer research · 2025
    Article
  6. Article
  7. The role of SIRT1 in the development of gastrointestinal tumors.Frontiers in cell and developmental biology · 2025
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. PROX1-mediated epigenetic silencing ofInternational journal of biological sciences · 2023
    Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article
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

7 authors at 5 institutions in 2 countries.

E J YuDepartment of Health Sciences and Technology, Samsung Advanced Institute for Health Sciences and Technology, Sungkyunkwan University, Samsung Cancer Center, Seoul, Korea.
S-H KimDepartment of Health Sciences and Technology, Samsung Advanced Institute for Health Sciences and Technology, Sungkyunkwan University, Samsung Cancer Center, Seoul, Korea.
H J KimDepartment of Health Sciences and Technology, Samsung Advanced Institute for Health Sciences and Technology, Sungkyunkwan University, Samsung Cancer Center, Seoul, Korea.
K HeoDepartment of Clinical Research, Dongnam Institute of Radiological and Medical Sciences, Busan, Korea.
C-Y OuDepartment of Biochemistry and Molecular Biology, University of Southern California, Los Angeles, CA, USA.
M R StallcupDepartment of Biochemistry and Molecular Biology, University of Southern California, Los Angeles, CA, USA.
J H KimDepartment of Health Sciences and Technology, Samsung Advanced Institute for Health Sciences and Technology, Sungkyunkwan University, Samsung Cancer Center, Seoul, Korea.
Samsung Medical Center · KRUniversity of Southern California · USDongnam Institute of Radiological & Medical Sciences · KRSamsung (South Korea) · KRSungkyunkwan University · KR

Funding

USC/NORRIS COMPREHENSIVE CANCER CENTER (CORE) SUPPORTP30CA014089 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI Fumito Ito · 1985 to 2026
$181.4M
Transcription activation by nuclear coactivatorsR01DK043093 · NIDDK · UNIVERSITY OF SOUTHERN CALIFORNIA · PI STALLCUP, MICHAEL R · 1990 to 2019
$6.5M
NCI NIH HHS P30 CA014089NIDDK NIH HHS R01 DK043093
6 · The paper itself

Abstract

Aberrant activation of Wnt/β-catenin pathway contributes to colorectal cancer (CRC) progression. However, little is known about regulatory mechanisms of the β-catenin activity in cancer progression. Here we investigated the role of DBC1, which was recently reported as a negative regulator of SIRT1 and a transcriptional coactivator, in the regulation of Wnt/β-catenin signaling. We identified the genome-wide targets of DBC1 and found that loss of DBC1 inhibits the expression of β-catenin target genes including PROX1, a transcription factor linked to CRC progression. Mechanistically, DBC1 stabilizes LEF1-β-catenin interaction by inhibiting SIRT1-mediated β-catenin deacetylation, thereby enhancing LEF1-β-catenin complex formation and long-range chromatin looping at the PROX1 locus. Furthermore, DBC1 is also required for the transcriptional activity of PROX1, suggesting that DBC1 has a dual function in regulating β-catenin-PROX1 signaling axis: as a coactivator for both β-catenin and PROX1. Importantly, loss of DBC1 inhibited growth and tumorigenic potential of colon cancer cells, and DBC1 expression correlated with shorter relapse-free survival in patients with advanced CRC. Our results firmly establish DBC1 as a critical positive regulator of β-catenin-PROX1 signaling axis and a key factor in β-catenin-PROX1-mediated CRC progression.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsbeta CateninCell LineCell Line, TumorColorectal NeoplasmsDisease ProgressionFemaleGene Expression Regulation, NeoplasticHEK293 CellsHomeodomain ProteinsHT29 CellsHumansImmunohistochemistryMice, Inbred BALB CMice, NudeAdaptor Proteins, Signal Transducingbeta CateninCCAR2 protein, humanHomeodomain ProteinsProspero-Related Homeobox 1 ProteinTumor Suppressor Proteins

Identifiers

PMID26477307
PMCPMC5058359
OpenAlexW1781506389

What OpenQuestion holds

Textmetadata
LicenceTDM
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.