Evidence map›Paper›PMID 22869582›Full record

ArticleCancer research2012

Prohibitin attenuates colitis-associated tumorigenesis in mice by modulating p53 and STAT3 apoptotic responses.

Arwa S Kathiria, William L Neumann, Jennifer Rhees, Erin Hotchkiss, Yulan Cheng, Robert M Genta, Stephen J Meltzer, Rhonda F Souza, Arianne L Theiss

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.7field-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

29 citing papers in PubMed, 63 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Prohibitions in the meta-inflammatory response: a review.Frontiers in molecular biosciences · 2024
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Bryostatin-1 ameliorated experimental colitis in Il-10Journal of cellular and molecular medicine · 2019
    Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Neuropeptide Y (NPY) promotes inflammation-induced tumorigenesis by enhancing epithelial cell proliferation.American journal of physiology. Gastrointestinal and liver physiology · 2017
    Article
  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

9 authors at 6 institutions in 1 country.

Arwa S KathiriaDepartment of Internal Medicine, Division of Gastroenterology, Baylor Research Institute, Baylor University Medical Center, Dallas, Texas 75246, USA.
William L Neumann
Jennifer Rhees
Erin Hotchkiss
Yulan Cheng
Robert M Genta
Stephen J Meltzer
Rhonda F Souza
Arianne L Theiss
Baylor University Medical Center · USSidney Kimmel Comprehensive Cancer Center · USJohns Hopkins University · USSouthwestern Medical Center · USThe University of Texas Southwestern Medical Center · USVA North Texas Health Care System · US

Funding

Inflammatory Bowel Disease-Associated Malignant TransformationR01CA133012 · NCI · JOHNS HOPKINS UNIVERSITY · PI MELTZER, STEPHEN J · 2009 to 2013
$1.5M
Role and function of prohibitin in intestinal inflammationK01DK085222 · NIDDK · EMORY UNIVERSITY · PI THEISS, ARIANNE L · 2010 to 2014
$671k
NCI NIH HHS R01 CA133012NCI NIH HHS R01-CA133012NIDDK NIH HHS K01 DK085222NIDDK NIH HHS K01-DK085222
6 · The paper itself

Abstract

Although inflammatory bowel disease is associated with higher risk of colorectal cancer, the precise pathogenic mechanisms underlying this association are not completely understood. Prohibitin 1 (PHB), a protein implicated in the regulation of proliferation, apoptosis, and transcription, is decreased in intestinal inflammation. In this study, we have established a key function for PHB in mediating colitis-associated cancer. Wild-type and transgenic (Tg) mice specifically overexpressing PHB in intestinal epithelial cells were subjected to a classical two-stage protocol of colitis-associated carcinogenesis. In addition, wild-type and p53 null human cell models were used to assess PHB interaction with STAT3 and p53. Wild-type mice exhibited decreased mucosal PHB protein expression during colitis-associated carcinogenesis. Tg mice exhibited decreased susceptibility in a manner associated with increased apoptosis, p53, Bax, and Bad expression plus decreased Bcl-xL and Bcl-2 expression. PHB overexpression in wild-type but not p53 null human cells increased expression of Bax, Bad, and caspase-3 cleavage. In wild-type p53 cells, PHB overexpression decreased basal and interleukin-6-induced STAT3 activation and expression of the STAT3 responsive genes Bcl-xL and Bcl-2. PHB coimmunoprecipitated with phospho-STAT3 in addition to p53 in cultured cell lysates and colon mucosa. This is the first study to show interaction between PHB and STAT3 in vivo. In summary, our findings suggest that PHB protects against colitis-associated cancer by modulating p53- and STAT3-mediated apoptosis. Modulation of PHB expression in intestinal epithelial cells may offer a potential therapeutic approach to prevent colitis-associated carcinogenesis.

Indexed as

AnimalsApoptosisCaco-2 CellsColitisColonic NeoplasmsDisease Models, AnimalFemaleHumansIntestinal MucosaMaleMiceMice, Inbred C57BLMice, TransgenicProhibitinsRepressor ProteinsSTAT3 Transcription FactorPHB protein, humanProhibitinsRepressor ProteinsStat3 protein, mouseSTAT3 Transcription FactorTumor Suppressor Protein p53

Identifiers

PMID22869582
PMCPMC3500430
OpenAlexW2093919096

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.