Evidence map›Paper›PMID 25887885›Full record

ArticleMolecular cancer therapeutics2015

Xanthohumol-Mediated Suppression of Notch1 Signaling Is Associated with Antitumor Activity in Human Pancreatic Cancer Cells.

Selvi Kunnimalaiyaan, Jose Trevino, Susan Tsai, T Clark Gamblin, Muthusamy Kunnimalaiyaan

Open access · greenAbstract read
In one paragraph

Article in Molecular cancer therapeutics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
8.8field-weighted citation impact, top 2% 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

22 citing papers in PubMed, 56 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Anticancer Potential of Natural Chalcones: In Vitro and In Vivo Evidence.International journal of molecular sciences · 2023
    Review
  6. Review
  7. Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Novel delivery approaches for cancer therapeutics.Journal of controlled release : official journal of the Controlled Release Society · 2015
    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

5 authors at 2 institutions in 1 country.

Selvi KunnimalaiyaanDivision of Surgical Oncology and Medical College of Wisconsin Cancer Center, Department of Surgery, Medical College of Wisconsin, Milwaukee, Wisconsin.
Jose TrevinoDepartment of Surgery, Section of Pancreatobiliary Surgery, University of Florida-Gainesville, Gainesville, Florida.
Susan TsaiDivision of Surgical Oncology and Medical College of Wisconsin Cancer Center, Department of Surgery, Medical College of Wisconsin, Milwaukee, Wisconsin.
T Clark GamblinDivision of Surgical Oncology and Medical College of Wisconsin Cancer Center, Department of Surgery, Medical College of Wisconsin, Milwaukee, Wisconsin.
Muthusamy KunnimalaiyaanDivision of Surgical Oncology and Medical College of Wisconsin Cancer Center, Department of Surgery, Medical College of Wisconsin, Milwaukee, Wisconsin. mkunnima@mcw.edu.
Medical College of Wisconsin · USUniversity of Florida · US

Funding

Role of GSK-3 isoforms in Pancreatic CancerR03CA155691 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI KUNNIMALAIYAAN, MUTHUSAMY · 2011 to 2012
$149k
NCI NIH HHS R03 CA 155691NCI NIH HHS R03 CA155691
6 · The paper itself

Abstract

Pancreatic cancer remains a lethal disease with limited treatment options. At the time of diagnosis, approximately 80% of these patients present with unresectable tumors caused by either locally advanced lesions or progressive metastatic growth. Therefore, development of novel treatment strategies and new therapeutics is needed. Xanthohumol (XN) has emerged as a potential compound that inhibits various types of cancer, but the molecular mechanism underlying the effects of XN remains unclear. In the present study, we have assessed the efficacy of XN on pancreatic cancer cell lines (AsPC-1, PANC-1, L3.6pl, MiaPaCa-2, 512, and 651) against cell growth in real time and using colony-forming assays. Treatment with XN resulted in reduction in cellular proliferation in a dose- and time-dependent manner. The growth suppression effect of XN in pancreatic cancer cell lines is due to increased apoptosis via the inhibition of the Notch1 signaling pathway, as evidenced by reduction in Notch1, HES-1, and survivin both at mRNA as well as protein levels. Notch1 promoter reporter analysis after XN treatment indicated that XN downregulates Notch promoter activity. Importantly, overexpression of active Notch1 in XN-treated pancreatic cancer cells resulted in negation of growth suppression. Taken together, these findings demonstrate, for the first time, that the growth suppressive effect of XN in pancreatic cancer cells is mainly mediated by Notch1 reduction.

Indexed as

Antineoplastic AgentsApoptosisBasic Helix-Loop-Helix ProteinsBlotting, WesternCell LineCell Line, TumorCell ProliferationCell SurvivalDose-Response Relationship, DrugFlavonoidsGene Expression Regulation, NeoplasticHomeodomain ProteinsHumansInhibitor of Apoptosis ProteinsPancreatic NeoplasmsPropiophenonesAntineoplastic AgentsBasic Helix-Loop-Helix ProteinsBIRC5 protein, humanFlavonoidsHES1 protein, humanHomeodomain ProteinsInhibitor of Apoptosis ProteinsNOTCH1 protein, humanPropiophenonesReceptor, Notch1SurvivinTranscription Factor HES-1xanthohumol

Identifiers

PMID25887885
PMCPMC4554525
OpenAlexW2003683047

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.