Evidence map›Paper›PMID 23339186›Full record

ArticleMolecular cancer research : MCR2013

Nuclear expression of β-catenin promotes RB stability and resistance to TNF-induced apoptosis in colon cancer cells.

Jinbo Han, Rossana C Soletti, Anil Sadarangani, Priya Sridevi, Michael E Ramirez, Lars Eckmann, Helena L Borges, Jean Y J Wang

Abstract read
In one paragraph

Article in Molecular cancer research : MCR, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

17 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Relevance of pRB Loss in Human Malignancies.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022
    Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. LATS2 inhibits the activity of NF-κ B signaling by disrupting the interaction between TAK1 and IKKβ.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. 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

8 authors at 2 institutions in 2 countries.

Jinbo HanMoores UCSD Cancer Center, University of California San Diego, La Jolla, California 92093, USA.
Rossana C Soletti
Anil Sadarangani
Priya Sridevi
Michael E Ramirez
Lars Eckmann
Helena L Borges
Jean Y J Wang
Universidade Federal do Rio de Janeiro · BRUniversity of California, San Diego · US

Funding

CELLULAR FUNCTION OF THE RETINOBLASTOMA GENE PRODUCTR01CA058320 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI WANG, JEAN Y.J. · 1992 to 2012
$4.0M
The UCSD Digestive Diseases Research Development CenterR24DK080506 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ECKMANN, LARS · 2008 to 2012
$2.7M
NCI NIH HHS R01 CA058320NCI NIH HHS R01CA058320NIDDK NIH HHS P30DK80506NIDDK NIH HHS R24 DK080506
6 · The paper itself

Abstract

Tumor necrosis factor (TNF)-α promotes tumor development under chronic inflammation. Because TNF also activates caspase-8, selective inhibition of TNF-induced extrinsic apoptosis would be required for inflammation-associated tumor growth. In a mouse model of inflammation-associated colon carcinogenesis, we found nuclear expression of β-catenin in tumors of wild-type, but not mutant, mice that were made resistant to TNF-induced apoptosis by a germline mutation blocking caspase cleavage of the retinoblastoma (RB) protein, despite similar frequencies of β-catenin exon-3 mutations in these two genetic backgrounds. TNF-induced apoptosis was also attenuated in human colon cancer cell lines with genetically activated β-catenin. However, we found that HCT116 cells, which contain an activated allele of β-catenin but do not express nuclear β-catenin, were sensitive to TNF-induced apoptosis. In HCT116 cells, TNF stimulated efficient RB cleavage that preceded chromatin condensation. In contrast, TNF did not induce RB cleavage in colon cancer cells expressing nuclear β-catenin and these cells could be sensitized to basal and/or TNF-induced apoptosis by the knockdown of β-catenin or RB. In the apoptosis-resistant colon cancer cells, knockdown of β-catenin led to a reduction in the RB protein without affecting RB mRNA. Furthermore, ectopic expression of the caspase-resistant, but not the wild-type, RB re-established resistance to TNF-induced caspase activation in colon cancer cells without β-catenin. Together, these results suggest that nuclear β-catenin-dependent RB stabilization suppresses TNF-induced apoptosis in caspase-8-positive colon cancer cells.

Indexed as

AnimalsApoptosisbeta CateninCaspase 8Cell NucleusColonic NeoplasmsGene Expression Regulation, NeoplasticGene Knockdown TechniquesHCT116 CellsHumansMiceRetinoblastoma ProteinSignal TransductionTumor Necrosis Factor-alphabeta CateninCaspase 8Retinoblastoma ProteinTumor Necrosis Factor-alpha

Identifiers

PMID23339186
PMCPMC4191841
OpenAlexW2140883369

What OpenQuestion holds

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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.